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EPILEPSY IN PREGNANCY

EPILEPSY IN PREGNANCY

Epilepsy is a chronic disorder characterized by recurrent, unpredictable seizures due to temporary dysfunction of the brain’s neurons producing excessive electrical discharge. 

Although it typically presents in childhood, it has a second peak in older adults, with women of childbearing age accounting for 23% of those affected. The prevalence of epilepsy in pregnancy is 0.35%.

Types of Epilepsy

Types of Epilepsy

A. Partial Epilepsy

1. Simple Partial Seizures:

  • Consciousness remains intact.
  • Experiences an aura (premonition).
  • Sensations like pins and needles in the arms or legs.
  • Pallor or a flushed face with sweating.
  • Muscle twisting in limbs with some stiffness.

2. Complex Partial Seizures:

  • Loss of memory of the event.
  • Hand rubbing.
  • Chewing and smacking of lips.
  • Random noises.
  • Unusual posture.

B. Generalized Epilepsy

1. Absence Seizures:

  • Staring and blinking.
  • Daydreaming with loss of awareness for 5-20 seconds (mainly affects children).

2. Myoclonic Seizures:

  • Brief muscle jerking in an arm or leg, lasting a fraction of a second while remaining conscious.
  • All body muscles contract for less than 20 seconds without convulsions, causing the individual to fall.

3. Tonic-Clonic Seizures:

  • Whole body contracts, arms and legs convulse.
  • Incontinence is possible.
  • Lasts 1-2 minutes, leaving the individual tired and wanting to sleep.
  • The most common type of seizure (60% of cases).

4. Atonic Seizures:

  • Sudden loss of muscle tone, causing the individual to fall limply.
  • Head injury is probable, but the individual gets up immediately with no confusion.

Causes of Epilepsy in Pregnancy

  1. Idiopathic: Most cases have no underlying cause.
  2. Genetic Predisposition: 30% of cases have a family history of epilepsy.
  3. Secondary Epilepsy: Can be encountered in pregnancy in patients with:
  • Previous brain surgery.
  • Intracranial mass lesions (e.g., meningiomas and arteriovenous malformations).
  • Antiphospholipid syndrome.

Other Causes of Seizures in Pregnancy

  • Eclampsia.
  • Cerebral vein thrombosis (CVT).
  • Thrombotic thrombocytopenic purpura (TTP).
  • Stroke.
  • Subarachnoid hemorrhage.
  • Drug and alcohol withdrawal.
  • Hypoglycemia.
  • Infections (e.g., tuberculoma, toxoplasmosis).
  • Gestational epilepsy (seizures confined to pregnancy).

Diagnosis

Most women are already diagnosed with epilepsy. However, if a first seizure occurs during pregnancy, the following investigations are appropriate:

  • Blood pressure, urinalysis, platelet count, clotting screen, blood film.
  • Blood glucose, serum calcium, serum sodium, liver function tests.
  • CT or MRI of the brain.
  • EEG (electroencephalogram).

Effects of Epilepsy on Pregnancy

On the Fetus:

  • No increased risk of miscarriage or obstetric complications unless a seizure results in abdominal trauma. This is a positive aspect, indicating that epilepsy itself doesn’t inherently increase the risk of these complications.
  • Fetal malformations: These can include a range of abnormalities affecting various organs and systems.
  • Intrauterine growth restriction (IUGR): This refers to the fetus not growing at the expected rate, potentially leading to low birth weight.
  • Oligohydramnios: This is a condition where there is too little amniotic fluid surrounding the fetus, which can be associated with developmental issues.
  • Preeclampsia: This is a serious condition characterized by high blood pressure and protein in the urine, which can affect both mother and fetus.
  • Stillbirths: This refers to the death of a fetus before birth.

On the Newborn:

  • Birth defects are increased two-fold. This could be related to the severity of the disease and also due to the anticonvulsants used. Pattern of abnormalities is related to the type of anticonvulsant drugs (valproate 5.9%, Carbamazepine, 2.3% and Lamotrigine 2.1%).
  • The malformations include—Cleft lip and/or palate, mental retardation, cardiac abnormalities, limb defects and hypoplasia of the terminal phalanges. Sodium valproate is associated with neural tube defects. 
  • There is chance of neonatal hemorrhage and is related to anticonvulsant induced reduction of coagulation factors (vitamin K dependent). The risk of developing epilepsy to the offspring of an epileptic mother is 10%.

On the Mother:

  • Increased risk of seizures during pregnancy and postpartum. Hormonal changes and physiological stress associated with pregnancy can trigger seizures.
  • Potential for worsening of epilepsy. Some women may experience an increase in seizure frequency or severity during pregnancy.
  • Difficulty in managing epilepsy medication during pregnancy. Many anticonvulsants are teratogenic (can cause birth defects), requiring careful consideration and monitoring.
  • Increased risk of postpartum depression. This can be exacerbated by the challenges of managing epilepsy and raising a child.

  • Stress and anxiety associated with pregnancy and childbirth. The fear of seizures and their potential impact on the baby can contribute to maternal stress.

Management of Epilepsy in Pregnancy

Pre-Pregnancy Counseling

1. Control of Epilepsy:

  • Maximize seizure control with the lowest dose of the most effective treatment.
  • Review antiepileptic drugs (AEDs) considering the risk of teratogenesis and adverse neurodevelopmental effects.

2. Stopping Treatment:

  • AEDs should be withdrawn slowly to reduce the risk of withdrawal-associated seizures, particularly important for benzodiazepines and phenobarbitone.
  • Current recommendations suggest stopping driving from the start of the drug withdrawal period and for six months after cessation of treatment if there are no seizures.

Newer Drugs with Safety Profiles:

  • Topiramate: 100–400 mg/day.
  • Levetiracetam: 1–3 gm/day, not an enzyme inducer.

Folic Acid: All women on AEDs should take pre-conception folic acid 4 mg daily starting before pregnancy and continuing throughout pregnancy.

Antenatal Management

1. Medication:

  • Keep the dose of chosen drugs as low as possible and monitor serum levels regularly.
  • Commonly used drugs include:
  1. Phenobarbitone (60-100mg daily in divided doses).
  2. Phenytoin (150-300mg daily in divided doses).
  3. Carbamazepine (0.8-1.2g daily in divided doses).
  • Continue folic acid daily before conception and throughout pregnancy to prevent folate-deficiency anemia.

2. Seizure Control:

  • IV Phenytoin: Administer a slow loading dose of 15–20 mg/kg for effective, long-duration control with fewer side effects.
  • Benzodiazepines: 10–20 mg slow IV if phenytoin is not effective.

3. Support:

  • Educate relatives, friends, and partners on placing the woman in the recovery position to prevent aspiration during a seizure.
  • Administer Vitamin K (10 mg daily) orally in the last two weeks of pregnancy.
  • Intrapartum Management

4. Seizure Risk:

  • The risk of seizures increases around delivery. Women with major convulsive seizures should deliver in a hospital.
  • Continue anticonvulsant medication throughout labor with regular review by the obstetric team.
  • Administer short-acting benzodiazepines if seizures recur.

5. Labor and Delivery:

  • Women should not be left alone during labor, and dehydration, hyperventilation, and exhaustion should be avoided as they can trigger seizures.

6. Vitamin K: 

  • 10 mg daily orally to the mother in the last two weeks of pregnancy.
  • Infant: 1 mg IM at birth to prevent neonatal hemorrhage
  • Birth can be spontaneous, facilitated by the midwife. Administer vitamin K to the baby promptly after birth to protect against AED-induced hemorrhagic disease.
  • Caesarean section is only necessary for recurrent generalized seizures in late pregnancy or labor.

Postpartum Management

7. Seizure Risk:

  • The risk of seizures increases in the first 24 hours after birth, so the woman should remain in the hospital.
  • Encourage breastfeeding.
  • Monitor the baby closely and report any concerns to the pediatrician immediately.
  • Provide safety advice for caring for the baby in case of maternal seizures.

8. Breastfeeding:

  • There is no contraindication for breastfeeding.
  • Infant: May be drowsy due to medication.

9. Postpartum Management:

  • Readjustment of Anticonvulsant Dosage: Reduce to pre-pregnancy levels by 4–6 weeks postpartum.

10. Contraception:

  • Avoid steroidal contraceptives due to hepatic microsomal enzyme induction.

11. Risk to Infant:

  • The risk of having epilepsy in an infant born to a mother with a seizure disorder is four times higher compared to infants born to mothers without a seizure disorder.

Complications Associated with Epilepsy

  1. Trauma: During seizures, injuries such as tongue biting and head or limb injuries can occur.
  2. Status Epilepticus: A seizure lasting more than 30 minutes or a series of seizures without regaining consciousness between them.
  3. Sudden Unexpected Death in Epilepsy (SUDEP): An unexplained sudden death in a person with epilepsy.

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ASTHMA IN PREGNANCY

ASTHMA IN PREGNANCY

Asthma is a chronic respiratory disorder characterized by recurrent attacks of wheezing and difficulty in breathing due to reversible narrowing of the airways. Asthma flare-ups during pregnancy can cause decreased oxygen in blood, which means less oxygen reaches the baby. This put the baby at higher risk for premature birth, low birth weight and poor growth.

Causes

The exact cause of asthma is unknown, but several predisposing factors contribute to its onset. These factors include:

Predisposing Factors

  1. Heredity: Asthma often runs in families, suggesting a genetic predisposition.
  2. Infections: Respiratory infections, such as the common cold, can trigger asthma attacks.
  3. Psychological Factors: Emotions like fear, anger, and nervousness can lead to the release of histamines, precipitating an asthma attack.
  4. Allergies: Common allergens include:
  • Foods
  • Pollen
  • Dust
  • Weather changes
  • Fungi
  • Spores
  • Feathers
  • Drugs (e.g., aspirin)

Respiratory Changes During Pregnancy

Anatomical Changes

  • Upper Respiratory Tract: Increased mucosal hyperemia, edema, and glandular hyperactivity.
  • Thorax and Diaphragm:

    • Subcostal Angle: Increases from 68 to 103 degrees in the first trimester.

    • Diaphragm: Rises by up to 4 cm.

Hormonal Effects on the Respiratory System

  • Oestrogen: Likely responsible for tissue edema, capillary congestion, and hyperplasia of mucous glands.
  • Progesterone: Contributes to improved asthma control through increased minute ventilation, smooth muscle relaxation, or cAMP-induced bronchodilation. However, it may also worsen asthma by altering beta2-adrenoceptor responsiveness and airway inflammation. Progesterone acts as a partial glucocorticoid agonist, suppressing histamine release from basophils.
  • Cortisol: Maternal plasma cortisol levels increase, which may improve asthma control and reduce steroid requirements, though the effects are variable.
  • Prostaglandins: Amniotic fluid contains various prostaglandins (PGE2, PGD2, PGF2-alpha). PGE2 is a bronchodilator, while others are bronchoconstrictors. The relationship between increased PGF2-alpha levels and asthma exacerbations is not well established.

Signs & Symptoms

History Taking

  • Family History: A family history of asthma, allergies, or frequent upper respiratory infections, particularly in the mother, increases the risk.
  • Personal History: A prior history of asthma, eczema, or hay fever can indicate a predisposition to asthma during pregnancy.
  • Onset: Sudden onset of wheezing, shortness of breath, and chest tightness, especially if it’s a new experience for the mother.
  • Triggers: Identifying known triggers such as dust, pollen, smoke, exercise, or certain medications can help manage the condition.
  • Severity: Determining the severity of past asthma episodes, including hospitalizations or emergency room visits, can inform treatment decisions.
  • Medications: Knowing current asthma medications, including inhalers and oral medications, and adherence to the treatment plan.

Examination

  • Cough: May be productive (with phlegm) or dry, often worse at night or during exercise.
  • Dyspnea: Difficulty breathing, shortness of breath, and feeling like you can’t get enough air.
  • Chest Tightness: A constricting or squeezing sensation in the chest.
  • Wheezing: High-pitched whistling sound during exhalation, sometimes heard during inhalation.
  • Rhonchi: Rattling or rumbling sounds in the chest, often indicating airway inflammation or mucus buildup.
  • Cyanosis: Bluish discoloration of the skin, lips, or fingernails, signifying low blood oxygen levels.
  • Accessory Muscle Use: Overuse of respiratory muscles in the neck, abdomen, or chest, to aid breathing, indicating significant respiratory effort.
  • Prolonged Expiration: Exhalation takes longer than inhalation due to narrowed airways.
  • Tachypnea: Rapid breathing rate.
  • Retractions: Pulling in of the chest wall or neck muscles during inhalation, a sign of respiratory distress.
  • Agitation: Restlessness, anxiety, or confusion, often associated with low blood oxygen levels.
  • Pulsus Paradoxus: A significant drop in blood pressure during inhalation, indicating severe airway narrowing.
Warning signs of Asthma Attack

History Findings:

  • Cough: A persistent cough, especially if it’s dry and hacking, can be an early sign.
  • Shortness of breath: Difficulty catching your breath, feeling like you can’t get enough air.
  • Chest tightness: A constricting feeling in the chest, making it difficult to breathe deeply.
  • Noisy breathing: Wheezing (high-pitched whistling sound), or rhonchi (rattling or rumbling sounds) during breathing.
  • Nocturnal awakenings: Waking up at night due to difficulty breathing.
  • Exacerbations possibly provoked by nonspecific stimuli: Triggers like dust, pollen, smoke, or exercise causing worsening symptoms.
  • Personal or family history of other atopic diseases: Having a history of allergies, eczema, or hay fever can increase the risk of asthma.

General Physical Examination:

  • Tachypnea: Rapid breathing.
  • Retraction (sternomastoid, abdominal, pectoralis muscles): Muscles in the neck, abdomen, or chest pulling inwards during inhalation as the body tries to get more air.
  • Agitation: Restlessness, anxiety, or confusion, often a sign of hypoxia (low oxygen levels).
  • Pulsus paradoxus ( > 20 mm Hg): A significant drop in blood pressure during inhalation.

Pulmonary Findings:

  • Diffuse wheezes: Long, high-pitched whistling sounds on exhalation and sometimes inhalation.
  • Diffuse rhonchi: Short, high- or low-pitched rattling sounds during inhalation and/or exhalation.
  • Bronchovesicular sounds: Abnormal lung sounds indicating airway narrowing.

Signs of Fatigue and Near-Respiratory Arrest:

  • Alteration in the level of consciousness: Lethargy, drowsiness, or confusion, indicating respiratory acidosis and fatigue.
  • Abdominal breathing: Using the abdominal muscles to help with breathing, a sign of respiratory distress.
  • Inability to speak in complete sentences: Speaking in short, choppy phrases due to shortness of breath.

Signs of Complicated Asthma:

  • Equality of breath sounds: Checking for equal air movement on both sides of the chest (signs of pneumonia, mucous plugs, or barotrauma).
  • A silent chest: The absence of wheezing in someone experiencing respiratory distress can be more worrisome than the presence of wheezing.
  • Jugular venous distension: Swelling of the neck veins, suggesting increased pressure in the chest cavity (possible pneumothorax).
  • Hypotension and tachycardia: Low blood pressure and fast heart rate, suggesting possible tension pneumothorax.
  • Fever: May indicate an upper or lower respiratory infection, which can worsen asthma symptoms.

Management of Asthma in Pregnancy

Aims of Management

  • Control symptoms, including nocturnal symptoms.
  • Prevent acute exacerbations.
  • Ensure no limitations on activities.
  • Maintain (near) normal pulmonary function.
  • Protect the mother and fetus from adverse effects.

Preventive Measures

When the patient is not experiencing an attack, prevention is very important. The following advice is given:

  1. Education: Inform the patient about asthma and identify potential triggers.
  2. Avoidance of Triggers: Avoid substances that trigger attacks (varies by individual).
  3. Warm Clothing: Use warm clothes, such as scarves, in cold weather.
  4. Emotional Control: Learn to manage emotions to prevent attacks.
  5. Deep Breathing Exercises: Practice exercises to ensure full lung expansion.
  6. Medication: Always have a supply of prescribed drugs (e.g., inhalers) according to the prescriptions.

Emergency Management

If the patient is experiencing an attack, treat it as an emergency:

  1. Admission: Quickly admit the patient in an upright position and administer oxygen if available.
  2. Reassurance: Reassure the patient and relatives to reduce anxiety, which can exacerbate the condition.
  3. Ventilation: Ensure proper ventilation and inform the doctor.
  4. Medical Treatment:
  5. Bronchodilators: Administer intravenous Aminophylline (250-500mg every 8 hours, given slowly over 20 minutes). Nebulized salbutamol (4mg every 8 hours), which may later be replaced with ordinary inhalers.
  • Corticosteroids: Hydrocortisone (100mg intravenously every 8 hours), later changed to oral prednisolone.
  • Antihistamines: Piriton or Phenergan to reduce allergic reactions and congestion.
  • Antibiotics: Crystalline penicillin (2ml every 6 hours) or Ampicillin (500mg every 6 hours) to prevent or treat respiratory infections.
  • Intravenous Fluids: Administer dextrose 5% to prevent dehydration and provide energy.

Quick Relief for All Patients

  • Short-acting bronchodilator: 2-4 puffs of short-acting inhaled beta-agonist(Such as Salbutamol) as needed for symptoms. Intensity of treatment depends on the severity of exacerbation; up to 3 times at 20-minute intervals or a single nebulizer treatment as needed. A course of systemic corticosteroids may be needed. Use of short-acting inhaled beta-agonist more than 2 times a week in intermittent asthma (daily, or increasing use in persistent asthma) may indicate the need to initiate or increase long-term control therapy.

Step Ladder Management

  1. Step 1: Occasional use of inhaled short-acting beta2-adrenoceptor agonist bronchodilators.
  2. Step 2: Introduction of regular preventer therapy, preferably inhaled corticosteroids (ICS).
  3. Step 3: Add-on therapy with long-acting beta2-agonists (LABAs), such as salmeterol and formoterol.
  4. Step 4: Poor control with Step 3: Addition of a fourth drug, such as leukotriene receptor antagonists or theophyllines.
  5. Step 5: Continuous or frequent use of oral steroids.

Non-Pharmacological Management

Patient Education

  • Explain that it is safer for pregnant women with asthma to take asthma medications than to have ongoing symptoms or exacerbations.
  • Reassure that safe and adequate asthma treatment is possible during pregnancy and that good asthma control minimizes the risk of complications.

Smoking Cessation

  • Smoking increases the risk of asthma exacerbations, bronchitis, or sinusitis, and necessitates an increased need for medication.
  • Associated with adverse pregnancy outcomes, including spontaneous pregnancy loss, placental abruption, preterm premature rupture of membranes (PPROM), placenta previa, preterm labor and delivery, low birth weight, and ectopic pregnancy.

Control of Environmental Triggers

  • Reduce the need for pharmacologic intervention by avoiding exposure to allergens and nonspecific airway irritants like tobacco smoke, dust, and environmental pollutants.
  • Particular allergens of concern include dander from pets and antigens from household dust mites.

Nursing Care

Bed Rest: Complete bed rest is essential, with assistance provided for all activities due to dyspnea.

  • Maternal Positioning: Pregnant patients with acute asthma should rest in a seated or lateral position to avoid aortocaval compression by the gravid uterus, particularly in the third trimester.
  • Hydration: Intravenous fluids are not necessary unless the patient cannot maintain oral hydration.
  • Supplemental Oxygen: Initially 3 to 4 L/min by nasal cannula, adjusting to maintain a PaO2 of at least 70 mmHg and/or oxygen saturation of 95% or greater.

  • Observation: Monitor fetal condition and mother’s response to treatment closely.

Management Of Acute Attacks Of Asthma (Asthma Exacerbation) In Pregnancy

  • Avoidance of asthma triggers (allergens, irritant) to minimize airway inflammation and hyper-responsiveness.
  • Oxygen inhalation with mask to maintain Oxygen saturation > 95% (pulse oximeter).
  • High dose albuterol by nebulization every 20 minutes and inhaled ipratropium bromide and systemic corticosteroid. 
  • Repeat assessment of symptom, physical examination and Oxygen  saturation to be done.
  • Corticosteroids: Intravenous hydrocortisone 200 mg stat and to be repeated after 4 hours. Because of long onset of action, corticosteroids should be given along with β2-agonists. 
  • Mechanical ventilation is needed for status asthmaticus to avoid hypoxemia and carbon dioxide retention.

Pharmacotherapy in Exacerbations

  • Agents: The recommended agents include inhaled short-acting beta-agonists e.g Albuterol (ProAir, Ventolin), levalbuterol (Xopenex), terbutaline (Brethine). These are often given via nebulizer or metered-dose inhaler (MDI), inhaled anticholinergic agents e.g Ipratropium bromide (Atrovent), oral or intravenous glucocorticoids Oral prednisone or methylprednisolone (Solu-Medrol).
  • Systemic Glucocorticoids: Benefits outweigh risks in preventing life-threatening asthma exacerbations e.g Dexamethasone.
  • Ipratropium: Used to treat severe acute asthma exacerbations.
  • Intravenous Magnesium Sulfate: Magnesium sulfate can be used in severe, life-threatening asthma exacerbations, especially in those who haven’t responded well to other treatments. It has bronchodilating and anti-inflammatory effects.

Asthma Management During Labor and Delivery

  • Only 10-20% of women develop an exacerbation during labor and delivery.
  • Opiate analgesics should be avoided as they are bronchoconstrictor and respiratory depressant. Maternal oxygenation should be adequately maintained. Labetalol should be avoided as it may precipitate asthma.
  • Hydrocortisone 100 mg IV 8 hourly during labor and 24 hours postpartum is to be given if the patient had steroids within the previous 4 weeks. Inhaled corticosteroid (fluticasone, budesonide) prevents bronchial hyper-responsiveness to allergens.
  • Syntocinon is better than ergometrine because of bronchoconstrictor effect of the latter. PGF2 α should not be used, as it precipitates bronchospasm. PGE1 and PGE2 compounds can be used locally for induction of labour or abortion.
  • Epidural anesthesia is preferable to general anesthesia because of risk of atelectasis and subsequent chest infection following the latter. Halothane is better in general anesthesia. However, it produces uterine atony.
  • Ketamine is used for induction of general anesthesia as it prevents bronchospasm.
  • Oxygen saturation is assessed with pulse oximeter or arterial blood gases.
  • Postnatal physiotherapy is maintained and drugs are continued.
  • Breastfeeding should be encouraged, as it delays the onset of allergic problems in the child. Drugs used in asthma: Prednisolone, corticosteroids, LABA, LTRA do not contraindicate breast feeding.
  • Contraception: Barrier method is the best. For terminal contraception, husband is to be motivated for vasectomy.

Peripartum Care

  • Oxytocin: The drug of choice for labor induction and postpartum hemorrhage control.
  • Pain Control: Avoid morphine and meperidine; use fentanyl or butorphanol. Epidural anesthesia is preferred; if general anesthesia is needed, use ketamine due to its bronchodilatory effect. Avoid ergot derivatives.
  • Monitoring: Monitor blood glucose levels in the baby if high doses of short-acting beta-agonists were used during labor and delivery.

Effects of Asthma on Pregnancy

  1. Infections: Increased susceptibility due to lowered resistance.
  2. Physiological Changes: Nervous system changes can lead to frequent attacks.
  3. Complications:
  • Exhaustion, stress, cyanosis, and dyspnea can cause intrauterine hypoxia.
  • Rapid pulse, tachypnea, and lowered blood pressure.
  • Mental confusion due to reduced oxygen to the brain.
  • Placental insufficiency leading to intrauterine growth retardation.

Maternal Risks:

  • Hyperemesis (severe nausea and vomiting): Asthma medications, particularly inhaled corticosteroids, can contribute to nausea and vomiting.
  • Accidental haemorrhage: Increased risk of bleeding during pregnancy since some asthma features can predispose mother to trauma.
  • Respiratory failure: Severe asthma attacks can lead to respiratory failure, requiring mechanical ventilation.
  • Pregnancy-induced hypertension (PIH): Asthma may increase the risk of developing PIH, a serious condition characterized by high blood pressure during pregnancy.
  • Preterm labour and premature birth: Asthma exacerbations can trigger contractions and lead to early delivery.
  • Increased risk of maternal death: Severe asthma complications, particularly respiratory failure, can be life-threatening.

Effects on Labor

  • Status Asthmaticus: An attack that does not respond to usual treatment.
  • Fetal Asphyxia: Due to constriction of blood vessels in the lungs.
  • Maternal Distress: Significant distress and potential obstetric shock.
  • Assisted Delivery: Necessary due to the mother’s inability to push effectively.

Effects on the Baby

  1. Oligohydramnios (low amniotic fluid levels): Asthma medications can affect the baby’s fluid balance, potentially leading to low amniotic fluid.
  2. Low birth weight (LBW): Premature birth, which is more common in women with asthma, is a major factor contributing to LBW.
  3. Premature delivery: Asthma can increase the chances of delivering before the full term of pregnancy.
  4. Fetal demise (death): Severe asthma complications, particularly during the third trimester, can lead to fetal distress and death.
  5. Meconium staining (indicating fetal distress): Fetal distress can cause the baby to release meconium (first stool) into the amniotic fluid.

Neonatal Risks:

  1. Neonatal hypoxemia (low oxygen levels): Premature babies born to mothers with asthma are more likely to experience low oxygen levels at birth.
  2. Low newborn assessment scores: Prematurity and low oxygen levels can negatively impact the baby’s apgar score.
  3. Increased perinatal mortality: Premature birth and complications associated with asthma can increase the risk of infant death.

Complications

  1. Cardiac Failure: Due to the increased strain on the heart.
  2. Respiratory Failure: Severe and untreated attacks can lead to respiratory failure.
  3. Poor Lactation: Due to the physical stress and medication.
  4. Chronic Bronchitis: Frequent attacks may lead to chronic bronchitis.
  5. Atonic Uterus: Resulting in prolonged labor or postpartum hemorrhage.
  6. Abortions and Premature Labor: Due to the stress and physical demands of asthma.
  7. Neonatal Complications: Various complications can arise due to the mother’s condition.

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ESSENTIAL HYPERTENSION IN PREGNANCY

ESSENTIAL HYPERTENSION IN PREGNANCY 

Apart from Pregnancy Induced Hypertension (PIH), Essential Hypertension is the most common hypertensive state in pregnancy. This is primary hypertension where the blood pressure is raised over 140/90mmHg during the first 20 weeks of pregnancy. It’s usually present before pregnancy. It doesn’t present with any proteinuria as in severe preeclampsia.

Essential hypertension in pregnancy refers to high blood pressure that develops before pregnancy or within the first 20 weeks of gestation and persists throughout pregnancy.

Classifications of Essential Hypertension

Hypertension, or high blood pressure, can be categorized into three levels based on the diastolic blood pressure reading:

  1. Mild Hypertension: Diastolic blood pressure between 95 and 105 mmHg.
  2. Moderate Hypertension: Diastolic blood pressure between 105 and 115 mmHg.
  3. Severe Hypertension: Diastolic blood pressure above 115 mmHg.

Causes of Essential Hypertension

The exact causes of essential hypertension are not fully understood. 

Factors that may contribute to the development of essential hypertension include;

1. Genetics: Family history of hypertension significantly increases the risk. Studies have identified specific genes associated with the condition.

2. Lifestyle Factors:

  • High Sodium Intake: Excessive salt consumption can contribute to fluid retention and increased blood pressure.
  • Low Potassium Intake: Adequate potassium is essential for regulating blood pressure, and low levels can contribute to hypertension.
  • Obesity: Excess body weight increases the workload on the heart and blood vessels, leading to higher blood pressure.
  • Physical Inactivity: Lack of regular exercise can contribute to weight gain and cardiovascular problems, including hypertension.
  • Smoking: Nicotine constricts blood vessels, raising blood pressure.
  • Excessive Alcohol Consumption: Heavy drinking can damage blood vessels and increase blood pressure.
  • Stress: Chronic stress can trigger the release of hormones that increase blood pressure.

3. Underlying Medical Conditions:

  • Kidney Disease: Kidney problems can impair the body’s ability to regulate blood pressure.
  • Thyroid Disorders: Hyperthyroidism can lead to increased heart rate and blood pressure.
  • Sleep Apnea: Disrupted sleep patterns can raise blood pressure.
  • Diabetes: Diabetes can damage blood vessels and increase the risk of hypertension.

SIGNS AND SYMPTOMS

Essential hypertension is often referred to as the “silent killer” because it most of the time doesn’t cause noticeable symptoms in its early stages. This makes it even more dangerous because damage to the heart, blood vessels, and other organs can occur without any warning signs.

  • Raised blood pressure of 140/90mmHg or more in early pregnancy: This indicates elevated blood pressure readings, specifically a systolic pressure (top number) of 140 mmHg or higher and/or a diastolic pressure (bottom number) of 90 mmHg or higher. 
  • Headaches: High blood pressure can cause persistent, throbbing headaches, often at the back of the head or temples.
  • Shortness of breath: Hypertension can lead to fluid buildup in the lungs, making it difficult to breathe.
  • Chest discomfort: The strain on the heart from high blood pressure can cause chest pain or tightness.
  • Sleep disturbances: Hypertension may contribute to sleep apnea and other sleep problems.
  • Palpitations and tachycardias: High blood pressure can cause an irregular or rapid heartbeat.
  • Fluid retention: Hypertension can lead to fluid buildup in the body, causing swelling in the legs, ankles, and feet.
  • Blurred vision: Damage to the blood vessels in the eyes is a potential complication of hypertension. 
  • Nausea or vomiting: Nausea and vomiting in hypertensive pregnancies can occur due to generalized malaise or as a response to the stress placed on the body by elevated blood pressure.
  • Fatigue and loss of energy: The strain on the cardiovascular system from high blood pressure can lead to feelings of tiredness and low energy.

Management of Essential hypertension

Elevated blood pressure is usually caused by a combination of several abnormalities such as psychological stress, genetic inheritance, environmental and dietary factors and others. Patients in whom no specific cause of hypertension can be found are said to have essential hypertension or primary hypertension (accounts for 80-90 % of cases). 

The choice of therapy of a patient with hypertension depends on a variety of factors: age, sex, race, body build, life-style of the patient, cause of the disease, other coexisting disease, rapidity of onset and severity of hypertension, and the presence or absence of other risk factors for cardiovascular disease (e.g. smoking, alcohol consumption, obesity, and personality type).

The aims/principles of management are: 

  • To stabilize the blood pressure to below 130/90 mm Hg.
  • To prevent superimposition of preeclampsia.
  • To monitor maternal and fetal well-being.
  • To terminate the pregnancy at the optimal time.

History Taking:

  • A thorough history should be taken for all mothers in the ANC Clinic to rule out essential hypertension (HT) in families.
  • This helps in early identification and management of at-risk mothers.

Blood Pressure and Urine Testing:

  • Regular and careful monitoring of blood pressure (BP) and urine testing is essential.
  • This helps in the early detection of any deviations from normal parameters.

Condition Management:

  • This condition is managed in the maternity centre (m/c) by midwives.
  • All mothers with signs of hypertension should be referred to a hospital for further management.

Non pharmacological therapy of hypertension

  • Low sodium chloride diet  Weight reduction.
  • Exercise.
  • Cessation of smoking.
  • Psychological methods (relaxation, meditation …etc).
  • Dietary decrease in saturated fats.
  • Decrease in excessive consumption of alcohol.
Management in Hospital

Mild Cases

Blood Pressure Range:

  • Mild cases are defined by blood pressure between 140/90 mmHg and 150/100 mmHg.

Antenatal Clinic Visits:

  • Patients should attend the Antenatal Clinic regularly every two weeks and be seen by a doctor.
  • Close monitoring of blood pressure and urine for albumin is necessary.
  • Weight checks and observation for edema should be conducted at every visit.

Fetal Monitoring:

  • Fetal growth and well-being should be carefully monitored to ensure normal development.
  • Excessive weight gain in the mother increases the risk of pre-eclampsia.

Medication:

  • Hypertensive drugs are usually not necessary for mild cases.
  • A sedative like Phenobarbital 30-60 mg nocte may be prescribed to reduce anxiety and ensure adequate rest.

Admission and Rest:

  • Mother is admitted at 36 weeks for rest in preparation for labor.
  • If blood pressure rises above 150/100 mmHg or there is albumin in the urine, immediate admission is required.

Advice on Diet and Rest:

  • Reduce intake of fats and carbohydrates, and avoid additional salt.
  • Ensure 10 hours of rest at night and 2 hours in the afternoon.
  • Avoid alcohol, smoking, and constipation.

Severe Cases

Admission:

  • Mother is admitted to the hospital and the doctor is informed.
  • Routine history taking, observation, and examination are conducted.

Urine and Blood Tests:

  • A mid-stream urine test is conducted to rule out albumin and check for pus cells and white blood cells.
  • Blood tests for blood urea are also performed.

Observation for Edema:

  • Examination for the presence of edema is necessary.
  • The mother is put on complete bed rest.

Nursing Care

Bed Rest:

  • Mother remains in bed for most of the day, with occasional sitting for relaxation.
  • The midwife provides a bedpan and brings necessities to the mother.

Hygiene:

  • Bed baths and vulva toilets are carried out every 4 hours.
  • Position changes and treatment of pressure areas are done 4-hourly.
  • Oral hygiene is maintained every 4 hours.
  • Bed linen is changed daily.

Diet:

  • A salt-free, light, and nourishing diet with plenty of proteins is provided.
  • Strict control of fluid intake to reduce and prevent edema.

Observations:

  • Temperature, pulse, respiration, and BP are checked every 4 hours.
  • Daily urine checks to rule out edema.
  • Fetal heart rate and growth are checked twice daily to rule out anoxia and intrauterine fetal death.
  • Placenta functional tests for efficiency.

Medical Treatment

Hypertensive Drugs:

  • Methyldopa, is the drug of choice during pregnancy, effective and safe for the mother and fetus. (Dosages below)
  • Indomethacin or methyldopa 250-750 mg orally as per the doctor’s prescription.
  • Hydralazine 1-4 mg twice a day.
  • Sedatives like Valium 5-10 mg 8-hourly.
  • Diuretics like furosemide.
  • Nifedipine 5 mg sublingually.

Obstetrical Management

Labor Induction:

  • Hypertensive mothers are not allowed to carry pregnancy to term.
  • In mild to moderate cases, labor is induced at about 38 weeks of gestation.
  • In severe cases, labor is induced at about 36 weeks of gestation.

First Stage of Labor:

  • Careful observations at 30-minute intervals.
  • BP checked every 2 hours or more frequently as ordered by the doctor.
  • Fetal heart rate checked every 30 minutes.

Second Stage of Labor:

  • Preparation may include additional equipment like vacuum extraction.
  • A large episiotomy is given to prevent maternal exhaustion.
  • Caesarean section may be done if progress is slow to avoid eclampsia.

Third Stage of Labor:

  • Injection of morphine 15 mg upon completion of labor.
  • Pitocin 10 IU in a drip.

Effects of Hypertension During Pregnancy

  • Abortion
  • Pre-eclampsia: Frequent complication with development of edema and proteinuria.
  • Eclampsia
  • Abruptio Placenta
  • Maternal Mortality
  • Renal Complications: Acute renal failure.

Effects of Hypertension During Labor

  • Premature Labor
  • Eclampsia
  • Poor Progress: Assisted delivery by vacuum extraction.
  • Cerebral Damage
  • Heart Failure

Effects of Hypertension During Puerperium

  • Low Resistance to Infection
  • Anemia
  • Postpartum Hemorrhage
  • Fits

Effects of Hypertension on Baby

  • Intrauterine Fetal Growth Retardation: Due to placental insufficiency.
  • Prematurity
  • Hypoxia and Anoxia
  • Abruptio Placenta
  • Asphyxia at Birth: Due to maternal cyanosis.
  • Mental Retardation
  • Deformity

Nursing Care Plan for a Patient with Essential Hypertension

Assessment

Diagnosis

Planning (Goals/Expected Outcomes)

Implementation

Rationale

Evaluation

1. Elevated blood pressure reading of 150/95 mmHg.  

2. Complains of headache and dizziness. 

3. Family history of hypertension. 

4. Patient’s diet includes high sodium intake. 

5. Sedentary lifestyle.

Hypertension related to lifestyle factors and genetic predisposition evidenced by blood pressure reading of 150/95 mmHg.

Short Term: 

 – Reduce blood pressure to below 140/90 mmHg within one week. 

– Patient will verbalize understanding of the importance of dietary and lifestyle modifications within three days.  Intermediate Term:  

– Blood pressure maintained between 120/80 mmHg and 130/85 mmHg within one month. 

 Long Term:  – Patient will adopt a healthier lifestyle, including a balanced diet and regular exercise, to maintain blood pressure within normal limits (<120/80 mmHg) within six months.

– Monitor blood pressure twice daily and record readings. 

 – Educate patient on the DASH diet (Dietary Approaches to Stop Hypertension). 

 – Encourage reduction of sodium intake to less than 2,300 mg per day. 

 – Advise patient to engage in at least 30 minutes of moderate-intensity exercise, such as brisk walking, five days a week. 

 – Administer antihypertensive medications as prescribed by the doctor. 

 – Discuss stress management techniques, such as deep breathing exercises and meditation.

– Regular monitoring helps track progress and adjust interventions as needed. 

– The DASH diet is proven to reduce blood pressure. 

– Reducing sodium intake helps lower blood pressure. 

– Regular exercise strengthens the heart and improves blood circulation, which can lower blood pressure. 

– Medications help control blood pressure levels. 

– Stress management can reduce blood pressure by calming the nervous system.

– Blood pressure reduced to 138/88 mmHg within one week. 

– Patient accurately explains the importance of dietary and lifestyle changes after three days. 

– Blood pressure maintained at 125/82 mmHg after one month. 

– Patient reports regular adherence to a healthier lifestyle and maintains blood pressure at 118/78 mmHg after six months.

1. Complaints of headache and dizziness. 

2. Elevated blood pressure reading of 150/95 mmHg.

Acute pain related to increased blood pressure evidenced by patient complaints of headache.

Short Term: 

– Patient will report a decrease in headache severity within one hour of intervention. 

Intermediate Term: 

– Patient will report fewer headaches within one month.

– Assess pain level using a 0-10 pain scale. 

– Administer prescribed analgesics for headache relief. 

– Encourage rest in a quiet, dark room. 

– Teach relaxation techniques, such as deep breathing or guided imagery.

– Pain assessment helps in determining the effectiveness of interventions. 

– Analgesics can provide immediate relief from headache. 

– A quiet environment reduces stimuli that may exacerbate headache. 

– Relaxation techniques can help reduce pain perception.

– Patient reports headache severity reduced from 8/10 to 2/10 within one hour. 

– Patient reports fewer and less severe headaches after one month.

1. Family history of hypertension. 

2. Elevated blood pressure reading of 150/95 mmHg.

Knowledge deficit related to lack of information about hypertension management evidenced by patient questions about diet and exercise.

Short Term: 

– Patient will demonstrate understanding of hypertension management by correctly answering questions about diet and exercise within one week. 

Long Term: 

– Patient will implement lifestyle changes to manage hypertension within three months.

– Provide educational materials on hypertension and its management. 

– Review the importance of medication adherence. 

– Demonstrate how to monitor blood pressure at home. 

– Discuss the role of diet, exercise, and stress management in controlling blood pressure.

– Education empowers the patient to take an active role in managing their condition. 

– Understanding medication importance improves adherence. 

– Home monitoring provides immediate feedback on lifestyle changes. 

– Knowledge of lifestyle factors helps in making informed decisions.

– Patient correctly answers questions about diet and exercise within one week. 

– Patient implements and adheres to recommended lifestyle changes, as evidenced by improved blood pressure readings within three months.

1. Patient’s diet includes high sodium intake. 

2. Elevated blood pressure reading of 150/95 mmHg.

Imbalanced nutrition: more than body requirements related to excessive sodium intake evidenced by elevated blood pressure.

Short Term: 

– Patient will identify high-sodium foods to avoid within one week. 

Intermediate Term: 

– Patient will reduce daily sodium intake to less than 2,300 mg within one month.

– Provide a list of high-sodium foods to avoid. 

– Teach label reading to identify sodium content in packaged foods. 

– Suggest healthier food alternatives. 

– Encourage cooking at home using fresh ingredients.

– Identifying high-sodium foods helps in making healthier choices. 

– Label reading educates on hidden sodium sources. 

– Healthier alternatives can reduce overall sodium intake. 

– Home-cooked meals allow better control of ingredients.

– Patient identifies high-sodium foods correctly within one week. 

– Patient reports reduced sodium intake and improved dietary habits within one month.

1. Sedentary lifestyle. 

2. Elevated blood pressure reading of 150/95 mmHg.

Activity intolerance related to sedentary lifestyle evidenced by complaints of fatigue and shortness of breath on exertion.

Short Term: 

– Patient will verbalize the importance of physical activity in managing hypertension within one week. 

Intermediate Term: 

– Patient will engage in 30 minutes of moderate-intensity exercise five days a week within one month.

– Assess current activity level and limitations. 

– Develop an individualized exercise plan starting with low-impact activities. 

– Encourage gradual increase in physical activity duration and intensity. 

– Monitor patient’s response to activity and adjust plan as needed.

– Understanding current activity level helps in setting realistic goals. 

– An individualized plan ensures activities are appropriate and safe. 

– Gradual increase in activity prevents injury and encourages adherence. 

– Monitoring response ensures safety and effectiveness of the plan.

– Patient verbalizes understanding of the importance of physical activity within one week. 

– Patient consistently engages in regular exercise, as evidenced by improved stamina and blood pressure readings within one month.

 

Pharmacological Therapy of Hypertension

Most patients with hypertension require drug treatment to achieve a sustained reduction in blood pressure. Currently available drugs lower blood pressure by decreasing either cardiac output or total peripheral vascular resistance, or both.

Anti-hypertensive drugs are classified according to the principal regulatory site or mechanism on which they act. They include:

A) Diuretics

Diuretics lower blood pressure by depleting the body’s sodium and reducing blood volume. They are effective in lowering blood pressure by 10-15 mmHg in most patients. Diuretics include:

1. Thiazides and Related Drugs

  • Examples: hydrochlorothiazide, bendrofluazide, chlorthalidone
  • Mechanism: Initially, thiazide diuretics reduce blood pressure by reducing blood volume and cardiac output due to increased urinary water and electrolyte (particularly sodium) excretion. With chronic administration (6-8 weeks), they decrease blood pressure by decreasing peripheral vascular resistance as the cardiac output and blood volume return to normal values.

2. Loop Diuretics

  • Examples: furosemide, ethacrynic acid
  • Mechanism: Loop diuretics are more potent than thiazides. The antihypertensive effect is mainly due to the reduction of blood volume. They are indicated in cases of severe hypertension associated with renal failure, heart failure, or liver cirrhosis.

3. Potassium-Sparing Diuretics

  • Examples: spironolactone
  • Mechanism: Used as adjuncts with thiazides or loop diuretics to avoid excessive potassium depletion and enhance the effect of other diuretics. The diuretic action of these drugs is weak when administered alone.

B) Direct Vasodilators

These include arterial vasodilators and arteriovenous vasodilators.

1. Arterial Vasodilators

  • Example: hydralazine
  • Mechanism: Dilates arterioles but not veins. It is used particularly in severe hypertension.
  • Side Effects: Common adverse effects include headache, nausea, anorexia, palpitations, sweating, and flushing.

2. Arteriovenous Vasodilators

  • Example: sodium nitroprusside

METHYLDOPA

  • Mechanism of Action: Central/peripheral antiadrenergic action resulting in decreased arterial pressure.
  • Dose: 250 mg – 500 mg orally.
  • Indications: Hypertension, pre-eclampsia.
  • Contraindications: Hepatic disorders, psychiatric patients, congestive heart failure, postpartum depression.
  • Side Effects: Hemolytic anemia, sodium retention, nausea, vomiting, diarrhea, constipation, weight gain, depression, dizziness, headache, fetal intestinal ileus.
  • Nursing Considerations:
  1. Monitor blood values of neutrophils and platelets.
  2. Monitor blood pressure before beginning treatment, periodically, and after.
  • Patient Instructions:
  1. Store tablets in tight containers.
  2. Avoid hazardous activities.
  3. Take the tablet one hour before meals.
  4. Do not stop the drug unless directed by a physician.
  5. Rise slowly to minimize orthostatic hypotension.

HYDRALAZINE

  • Mechanism of Action: Peripheral vasodilation as it relaxes the arterial smooth muscles. It increases cardiac output and renal blood flow.
  • Indications: Essential hypertension.
  • Dose:
  1. Orally: 100 mg/day in 4 divided doses.
  2. Intravenously: 5-10 mg every 20 minutes with a maximum of 20 mg.
  • Side Effects: Hypotension, tachycardia, fluid retention, muscle cramps, headache, depression, anorexia, diarrhea, neonatal thrombocytopenia.
  • Contraindications: Rheumatic heart disease.
  • Nursing Considerations:
  1. Monitor BP every 15 minutes for 2 hours, then hourly for 2 hours, then 4-hourly.
  2. Monitor fluid intake and output.
  3. Take weight daily.
  4. Administer in a recumbent position and keep the patient in that position for 1 hour after administration.
  5. Evaluate for edema, assess skin turgor, and monitor for dyspnea, orthopnea, joint pains, headaches, and palpitations.
  • Patient Instructions:
  1. Take with food to increase bioavailability.
  2. Notify the doctor if there is chest pain, severe fatigue, muscle or joint pains.

LABETALOL

  • Mechanism of Action: Decreases systemic arterial blood pressure and systemic vascular resistance due to its combined alpha and beta-adrenergic blocking activity.
  • Indications: Hypertension, hypertensive emergencies.
  • Dose:
  1. Orally: 100 mg three times daily.
  2. IV infusion: 20-40 mg every 10-15 minutes until the desired effect is achieved in a hypertensive crisis.
  • Contraindications: Hepatic disorders, asthma, congestive heart failure.
  • Side Effects: Tremors, headache, asthma, congestive cardiac failure, sodium retention, postural hypotension.
  • Nursing Considerations:
  1. Assess urine input and output.
  2. Take weight daily.
  3. If given intravenously, keep the patient in a recumbent position for 3 hours.
  4. Check for edema of legs and feet.
  5. Assess skin turgor and mucous membrane dryness for hydration status.
  • Patient Instructions:
  1. Take the tablet orally before food.
  2. Do not discontinue the drug abruptly.
  3. Report bradycardia, dizziness, confusion, or depression.
  4. Avoid alcohol, smoking, and excess sodium intake.
  5. Take medication at bedtime to prevent the effect of orthostatic hypotension.

NIFEDIPINE

  • Mechanism of Action: Dihydropyridine calcium channel blocker. Direct arterial vasodilator by inhibiting the slow inward calcium channel in vascular smooth muscles. Reduces muscle contractility.
  • Dose:
  1. Orally: 5-10 mg three times daily.
  2. Tocolytic dose: Initial dose of 20 mg orally, followed by 20 mg orally after 30 minutes. If contractions persist, continue with 20 mg orally every 3-8 hours for 48-72 hours with a maximum dose of 160 mg/day. Long-acting nifedipine (30-60 mg daily) can be used after 72 hours if maintenance is still required.
  • Indications: Hypertension, angina pectoris, preterm labor.
  • Contraindications: Simultaneous use with magnesium sulfate due to synergistic effects.
  • Side Effects: Flushing, hypotension, headache, tachycardia, inhibition of labor, fatigue, nausea and vomiting, drowsiness.
  • Nursing Considerations: Administer before meals.
  • Patient Instructions: Limit caffeine consumption.

PROPRANOLOL

  • Mechanism of Action: Sympatholytic non-selective beta-blocker that decreases preload and afterload, reducing left ventricular end-diastolic pressure and systemic vascular resistance.
  • Indications: Hypertension.
  • Contraindications: Bronchial asthma, diabetes mellitus, cardiac failure.
  • Side Effects: Severe hypotension, sodium retention, bradycardia, bronchospasms, intrauterine growth restriction (IUGR) with prolonged therapy, headache.
  • Dose: 80-240 mg once daily orally.
  • Nursing Considerations:
  1. Assess BP, pulse, and respirations during treatment therapy.
  2. Take weight often and report excess weight gain.
  3. Evaluate tolerance if taken for long periods.
  4. Evaluate for headaches.
  • Patient Instructions:
  1. Take with plenty of water on an empty stomach.
  2. Make position changes slowly to prevent fainting.

Common Diuretics Used

FRUSEMIDE

  • Type: Loop diuretic.
  • Mechanism of Action: Acts on the loop of Henle to prevent the reabsorption of sodium and potassium.
  • Dose:
  1. Oral: 10 mg/mL, 40 mg/5 mL.
  2. Injection: 10 mg/mL.
  3. Tablet: 20 mg, 40 mg, 80 mg.
  • Indications: Pregnancy-induced hypertension, eclampsia with pulmonary edema.
  • Contraindications: Anuria, hypersensitivity to the drug.
  • Side Effects: Fatigue, muscle cramps, hypokalemia, fetal compromise.

Anticonvulsants

Magnesium Sulphate

  • Mechanism of Action: Competitive inhibition to calcium ions either at the motor end plate or at the cell membrane, reducing calcium influx and directly acting on uterine muscles and motor plate sensitivity.
  • Indications: Premature rupture of membranes, active labor, planned delivery within 24 hours, prevention or control of seizures in pre-eclampsia, hypomagnesemia.
  • Dose Regimen:
  1. Loading Dose: 
  2. Maintenance Dose: 5 g IM 4 hourly on alternate buttocks, or 1-2 g/hr IV infusion.

  • Route of Administration

    Loading Dose

    Maintenance Dose

    Intramuscular

    4 g IV over 3-5 minutes, followed by 10 g deep IM.

    5g 4 hourly on alternate buttocks

    Intravenous

    4-6g i.v over 15-20 minutes

    1-2 g/hr i.v infusion

 

  • Side Effects: Flushing, nausea, vomiting, headache, blurred vision, respiratory depression.
  • Contraindications: Impaired renal function.

Diazepam

  • Mechanism of Action: Depresses subcortical levels of the CNS.
  • Dose:
  1. Orally: 2-10 mg three to four times daily.
  2. IV: 5-20 mg bolus, may repeat in 30 minutes if seizures reappear.
  • Side Effects: Hypotension, dizziness, drowsiness, headache, respiratory depression, birth hypotonia, thermoregulatory problems in the newborn.

Phenytoin

  • Mechanism of Action: Prolongs the inactivation state of sodium channels, reducing the likelihood of repetitive discharge.
  • Indications: Prevention and control of seizures in pre-eclampsia and eclampsia, status epilepticus.
  • Side Effects: Sedation, cleft palate (in fetuses).

Anticoagulants

Heparin Sodium

  • Mechanism of Action: Prevents the conversion of fibrinogen to fibrin.
  • Indications: Deep vein thrombosis, thromboembolism, disseminated intravascular coagulation, patients with prosthetic valves in the heart.
  • Action: Interferes with blood clotting by direct means, depressing hepatic synthesis of vitamin K-dependent coagulation factors.

Treatment of Shock

Shock is a clinical syndrome characterized by decreased blood supply to tissues. Signs and symptoms include oliguria, heart failure, disorientation, mental confusion, seizures, cold extremities, and coma. Most, but not all, people in shock are hypotensive. The treatment varies with the type of shock. The choice of drug depends primarily on the pathophysiology involved.

  • Anaphylactic Shock or Neurogenic Shock: Characterized by severe vasodilation and decreased PVR, a vasoconstrictor drug (e.g., levarterenol) is the first drug of choice.
  • Hypovolemic Shock: Intravenous fluids that replace the type of fluid lost should be given.
  • Septic Shock: Appropriate antibiotic therapy in addition to other treatment measures

ESSENTIAL HYPERTENSION IN PREGNANCY  Read More »

Renal Diseases in Pregnancy

Renal Diseases in Pregnancy

COMMON TERMS IN URINARY SYSTEM 

  •  Proteinuria: Daily excretion of proteins in the urine is more than 150mg. It signifies that the kidney is damaged/ perforated.
  • Haematuria: Means passing urine containing blood and is due to bleeding into the urinary tract.
  • Crystalluria : Presence of crystals like oxalates, phosphates in the urine detected by microscopic examination of urine
  • Glycosuria : Means presence of sugar (glucose) in urine either due to diabetes mellitus or due to renal glycosuria
  • Azotemia: Increase in the serum concentration of urea and creatinine above their normal values. This occurs when glomerular filtration pressure (GFR) of the kidneys falls due to renal failure. “uremia”.
  •  Oliguria : Diminished urine volume output of urine i.e. 100 mL to 400 mL  per day.
  •  Anuria – Complete absence of urine formation i.e zero to 100 mL per day
  •  Dysuria – Difficulty or pain in passing urine 
  •  Polyuria – Urine volume above 3 litres per day 
  •  Retention of urine – occurs due to obstruction of urine outflow from the bladder, this is relieved by catheterization

Anatomy of the Renal System 

The urinary system is the main excretory system eliminating waste products from blood through urine. Its anatomy consists of two kidneys, each joined to the bladder by the tube called ureter, which conveys urine from the kidneys to the bladder for storage. Following bladder contraction, urine is expelled through the urethra. 

The Kidneys

There are two kidneys which lie behind the peritoneum on either side of the vertebral column. In adults, they measure approximately 12 to 14 cm.

The urine is formed in the kidney by the nephrons. 

Each kidney has approximately one million nephrons. 

 

Role of the Kidneys 

• Influence blood pressure control 

• Release renin to activate the renin-angiotensin system 

• Can lead to water retention or excretion 

• Waste excretion(Urea, Creatinine, Uric Acid)

• Blood filtration

• Blood glucose regulation(glucose absorption)

• Acid Base Balance/pH regulation

• Electrolyte balance (Sodium, Potassium, Chloride)

•Erythropoiesis regulation(also produces Erythropoietin)

URINARY BLADDER

It is made up of four layers i.e. 

  •  Mucosa; this is the innermost layer with rugae that allows its distention. 

  •  Sub mucosa which provides rich vascular supply 

  •  Smooth muscle layer/ detrusor muscle; which contracts during urination  for urine expulsion.

  •  Serosa: a continuation of peritoneum 

 

The bladder has a triangular area called trigone with three openings at its angles i.e two for ureters laterally and one for the urethra at the apex

URETHRA

This conveys urine from the urinary bladder to outside of the body. 

The internal sphincter of smooth muscle and external urethral sphincter of skeletal muscles constricts the lumen of the urethra causing bladder to fill. 

Female urethra is 4cm long and male urethra is 20 cm

NEPHRON

This is a functional (urine) forming units of the kidneys

Components of the Nephron 

  • Bowman’s Capsule a cup-like structure made of squamous epithelium and inner layer has modified cell (podocytes) closely associated with glomerular capillaries 
  • Glomerulus made of highly permeable capillary network 
  • Proximal convoluted tubule, made of cuboidal epithelium with microvilli. It is a primary site of tubular reabsorption and secretion mechanisms. 
  • Loop of Henle, both ascending and descending loops are involved in urine concentration 
  • Distal Convoluted tubule; this is shorter than the proximal and contains macula densa specialized sensory cells which monitor NaCl concentrations. it’s a site of tubular reabsorption and secretion 
  • Collecting Ducts; these empty urine into the renal pyramids
 
Physiology of the urinary system  (1)

Physiology of the urinary system 

The volume of the urine excreted per day is about 1500m/s or roughly 1 ml /min. The processes responsible for urine formation are ultra filtration at the glomeruli and reabsorption in the tubules of the nephrons. 

The kidneys are largely responsible for maintaining this constancy and the excretion of waste products of metabolism. 

For example, urea which is a waste product of protein metabolism is excreted in a large quantity. Various renal functions are illustrated below 

 

FUNCTIONS OF THE RENAL SYSTEM 
  1.  Regulation of the water content of the body: About 2/3 of water filtered by the glomeruli is reabsorbed in the proximal tubules iso-osmotically.  The remaining water is reabsorbed in distal tubules and collecting duct; under the influence of antidiuretic hormone (ADH).
  2. Regulation of normal acid-base balance of the blood. The kidneys help to maintain a normal internal environment by preventing body fluids from becoming too acidic or too alkaline. 
  3.  Regulation of electrolyte content of the body. A large part of sodium ions (Na+), chloride ions (Cl- ) are actively reabsorbed in the PCT, DCT and collecting ducts. The kidney regulates the fluid balance by excreting more urine when a large amount of urine is taken and retains fluid when much has been lost. 
  4.  Hormonal and metabolic functions. The kidney produces many hormones which take part in various metabolic functions >Renin is produced in the “Juxta glomerular apparatus” and stimulates aldosterone secretion. 
  • > Erythropoietin – stimulates red blood cells production 
  • > Prostaglandins produced in the kidneys help in vasodilation of blood vessels.
Processes Involved in urine formation 
  • Filtration
  • Selective Reabsorption
  • Tubular Secretion
FILTRATION
This takes place through the semipermeable walls of the glomerulus and glomerular capsule/Bowman’s Capsule. Water and other small molecules pass through, although some are reabsorbed later. Blood cells, plasma proteins and other large molecules are too large to filter through and therefore remain in the capillaries.

Filtration takes place because there is a difference between the blood pressure in the glomerulus and the pressure of the filtrate in the glomerular capsule. 

Because the afferent arteriole is narrower than the afferent arteriole, a capillary hydrostatic pressure builds up in the glomerulus. This pressure is opposed by the osmotic pressure of the blood, provided mainly by plasma proteins, and by filtrate hydrostatic pressure in the glomerular capsule, 

The volume of filtrate formed by both kidneys each minute is called the glomerular filtration rate (GFR). In a healthy adult the GFR is about 125 ml/min, i.e. 180 liters of filtrate are formed each day by the two kidneys. Nearly all of the filtrate is later reabsorbed from the kidney tubules with less than 1%, i.e. 1 to 1.5 liters, excreted as urine. The differences in volume and concentration are due to selective reabsorption of some filtrate constituents and tubular secretion of others 

SELECTIVE REABSORPTION

Most reabsorption from the filtrate back into the blood takes place in the proximal convoluted tubule, whose walls are lined with microvilli to increase surface area for absorption.


 Materials essential to the body are reabsorbed here, including some water, electrolytes and organic nutrients such as glucose. Some reabsorption is passive, but some substances are transported actively. Only 60–70% of filtrate reaches the loop of the nephron.

 

Much of this, especially water, sodium and chloride, is reabsorbed in the loop, so only 15–20% of the original filtrate reaches the distal convoluted tubule, and the composition of the filtrate is now very different from its starting values. More electrolytes are reabsorbed here, especially sodium, so the filtrate entering the collecting ducts is actually quite dilute. The main function of the collecting ducts therefore is to reabsorb as much water as the body needs.

TUBULAR SECRETION

Filtration occurs as the blood flows through the glomerulus. 

Substances not required and foreign materials, e.g. drugs including penicillin and aspirin, may not be cleared from the blood by filtration because of the short time it remains in the glomerulus.

Such substances are cleared by secretion from the peritubular capillaries into the convoluted tubules and excreted from the body in the urine. 


Tubular secretion of hydrogen ions (H+) is important in maintaining normal blood pH.

Pyelonephritis in Pregnancy

Pyelonephritis in Pregnancy

Pyelonephritis is an infection of the kidneys, specifically affecting the renal pelvis and tubules.

 It occurs in approximately 2% of pregnant women, particularly during the second trimester (16-26th week), with a higher incidence in first-time mothers (primigravidas).

It is more common in;

  • Primigravidae than multiparae.
  • Previous history of urinary tract infection increases the chance by 50%.
  • Presence of asymptomatic bacteriuria increases the chance by 25%.
  • Abnormality in the renal tract is found in about 25%.

There is an increased chance of urinary tract infections (UTIs) in females compared to males due to:

  • Short urethra (4 cm): The female urethra is significantly shorter than the male urethra, making it easier for bacteria to ascend from the external opening to the bladder.
  • Close proximity of the external urethral meatus to areas (vulva and lower third of vagina) contaminated heavily with bacteria: The proximity of the urethra to areas harbouring a high concentration of bacteria increases the risk of contamination.
  • Catheterization: The use of urinary catheters, often for medical reasons, can introduce bacteria into the bladder and increase the risk of infection.
  • Sexual intercourse: Sexual intercourse can introduce bacteria into the urethra, particularly in women who are not properly lubricated.

Types of Infection:

  • Ascending Infection: Bacteria ascend from the bladder or urethra, often originating from neighbouring organs like the rectum.
  • Bloodborne Infection: Bacteria enter the bloodstream, often stemming from conditions like septicemia.

Causative Organisms for Pyelonephritis

  • E. coli (70%): The most common causative organism, usually originating from the gut.
  • Klebsiella pneumoniae (10%).
  • Enterobacter.
  • Proteus.
  • Pseudomonas.
  • Staphylococcus aureus group.

Predisposing Causes

  • Urinary Stasis: The growing uterus puts pressure on the ureters (tubes that carry urine from the kidneys to the bladder), causing them to dilate and kink. This creates areas where urine can pool, leading to stagnation and a favourable environment for bacterial growth.
  • Loss of Urethral Tone: Pregnancy hormones relax smooth muscles throughout the body, including the muscles surrounding the urethra. This loss of tone can contribute to urine stagnation and increased risk of infection.
  • Increased Vaginal Secretions: The increased production of vaginal discharge (leukorrhea) during pregnancy can introduce bacteria into the urethra, increasing the chances of infection.
  • Prior History of Nephritis: Women who had acute nephritis (kidney inflammation) in childhood are more susceptible to developing pyelonephritis during pregnancy. This suggests a predisposition to kidney infections.

Signs and Symptoms

  • Fever and Chills: A high fever (38-40°C) accompanied by chills is a common sign.
  • Painful and Frequent Urination: The inflammation of the urethra causes pain and increased frequency of urination, often with a burning sensation.
  • Tachycardia: An elevated heart rate (110-130 beats per minute or higher) is another typical sign.
  • Vomiting: Nausea and vomiting are frequent symptoms.
  • General Malaise: The patient may feel unwell with a coated tongue and overall weakness.
  • Offensive Urine: The urine may have a strong, unpleasant odor due to the presence of bacteria.
  • Epigastric Pain: Pain in the upper abdomen due to vomiting can also occur.
  • Tenderness on Examination: The doctor may find tenderness when examining the renal angles (the areas where the kidneys are located) and the area above the pubic bone.
  • Acute Aching Pain: A sharp, aching pain in the loins (lower back) is often felt, radiating to the groin and the costovertebral angle (the area where the ribs meet the spine).
  • Tenderness on Palpation: The costovertebral angle is often tender when pressed upon.
  • Urinary Symptoms: These include urgency (feeling like you need to urinate urgently), frequency (urinating more often than usual), dysuria (painful urination), and hematuria (blood in the urine).
  • Fever and Flu-like Symptoms: The fever can be high and spiky (reaching 40°C), with chills and rigors (muscle spasms). This may be followed by hypothermia (low body temperature, around 34°C). Other flu-like symptoms include anorexia (loss of appetite), nausea, vomiting, and myalgias (muscle aches).
  • Respiratory Distress: In severe cases, pyelonephritis can lead to respiratory distress and pulmonary edema (fluid in the lungs). This is due to endotoxin (a toxin released by bacteria) damaging the alveoli (tiny air sacs in the lungs). This is also known as Acute Respiratory Distress Syndrome (ARDS).

Diagnosis

A combination of factors aids in the diagnosis of pyelonephritis:

  • History: The patient’s history of painful urination, fever, and other symptoms is crucial.
  • Urinalysis: Examining the urine under a microscope reveals protein (from dead epithelial cells), sugar, and pus cells, all indicative of infection.
  • Urine Culture and Sensitivity: A culture of the urine helps identify the specific bacteria causing the infection. This information is crucial for selecting the appropriate antibiotic treatment.

Effects on Pregnancy

  • Increased Pregnancy Wastage: There is a higher risk of miscarriage or premature birth.
  • Abortions: The infection can trigger premature labor and lead to a miscarriage.
  • Premature Labor: Pyelonephritis can induce premature contractions and lead to early delivery.
  • Intrauterine Fetal Death: In severe cases, the infection can cause the fetus to die in the womb.
  • Small for Dates: The fetus may grow more slowly than expected due to the infection.
  • Accidental Haemorrhage: The infection can weaken the cervix and make it more prone to bleeding.
  • Anaemia: Pyelonephritis can contribute to anaemia due to the body’s response to infection.
  • Hypertension: The infection can elevate blood pressure, posing a risk to both the mother and fetus.
  • Septicemia and Septic Shock: The infection can spread to the bloodstream (septicemia), potentially leading to a life-threatening condition called septic shock.
  • Renal Dysfunction: Pyelonephritis can damage the kidneys, leading to impaired kidney function.

ACUTE PYELONEPHRITIS 

This is characterized by acute inflammation of the parenchyma(core substance of the kidney/kidney tissue) and the pelvis of the kidneys. 

The disease may be bilateral or unilateral. This usually results from untreated bacterial cystitis and may be associated with pregnancy, trauma of the urinary bladder, and urinary obstruction Also Ascending and Descending infections.

Presentation; flunk tenderness,

  • fever, chills 
  • Dysuria
  • Urgency
  • frequency

Chronic pyelonephritis 

This occurs due vesicoureteral reflux ( back flow of urine from the bladder to the ureters allowing spread of infection upwards to the kidneys. The condition is also called reflux nephropathy(This can lead to kidney distention called Hydronephrosis) 

It clinical presents with 

  • bacteriuria, 
  • hypertension, 
  • flunk tenderness,
  • septic shock, 
  • dizziness fainting and signs of renal insufficiency 

Management/Treatment of Pyelonephritis in Pregnancy

Aims of management

The management of pyelonephritis in pregnancy focuses on treating the infection and preventing further complications:

 

A midwife is permitted to treat mild pyelonephritis. If the temperature is 38oC or more, this won’t be mild, the patient must be transferred to hospital

Mild Pyelonephritis (Temperature Below 38°C):

Maternity Centre Management:

  • Fluid Intake: Encourage the mother to drink plenty of fluids.
  • Sulphadimidine: Administer sulphadimidine 2g stat, followed by 1g six-hourly for 5 days.
  • Nitrofurantoin: Prescribe nitrofurantoin 100mg six-hourly for 1 week.
  • Monitoring: Closely observe the patient’s progress. If no improvement is seen within 3 days, transfer to a hospital for further evaluation and management.

In hospital

  • Admission: Immediate hospitalization is required for patients with a temperature of 38°C or higher.
  • Bed Rest: Provide complete bed rest in a well-ventilated room.
  • Positioning: Encourage the mother to lie on the unaffected side.
  • Fluid Management: Ensure adequate fluid intake and monitor fluid balance closely.
  • Intravenous Fluids: Intravenous fluids (crystalloid solutions) are administered to ensure adequate hydration.
  • Monitoring: Urine output (greater than 60 ml/hour), temperature, and blood pressure are closely monitored
  • Vital Signs: Monitor vital signs (temperature, pulse rate, respiration, blood pressure) every four hours.
  • Blood Tests: Blood tests including a complete blood count (hemogram), serum electrolytes, and creatinine levels are performed to assess the patient’s health and kidney function.
  • Urine Testing: Test urine for albumin daily.
  • Dietary Management: As the patient improves, gradually introduce a light diet.
  • Fever Control: Administer tepid sponging as needed to reduce fever.
  • Constipation Management: Prescribe mild laxatives if constipation occurs.
  • Keep strict fluid balance chart.

Medical Treatment:

  • Antibiotic Therapy: Intravenous antibiotics are administered for 48 hours. Common choices include cephalosporins, aminoglycosides (gentamicin), Cefazolin, or Ceftriaxone. Once the culture results are available, the antibiotic may be switched to an oral therapy for another 10-14 days.
  • Repeat Cultures: Urine cultures are repeated after 2 weeks of antibiotic therapy and at each trimester of pregnancy.
  • Retreatment: If symptoms recur or the urine dipstick test for nitrate and leukocyte esterase is positive, a urine culture is repeated, and treatment is given if the culture is positive.
  • Imaging Studies: If the patient does not respond to treatment, imaging studies like ultrasound, CT scan, or radiography may be required to rule out urinary tract obstruction.
  • Antimicrobial Suppression Therapy: To prevent recurrence (which occurs in 30-40% of cases), antimicrobial suppression therapy may be continued until the end of pregnancy. Nitrofurantoin 100 mg daily at bedtime is an effective option.  Cephalexin 250–500 mg orally every day for the remainder of pregnancy and continuing until 4–6 weeks postpartum is also recommended if nitrofurantoin is not available.
  • Potassium Citrate: Prescribe potassium citrate 15 ml four-hourly to alkalinize the urine and potentially relieve pain.
  • Fever Management: Acetaminophen (paracetamol) is given to reduce fever.
  • Fluid Intake: There is a danger of crystallisation of these sulphur drugs to the kidneys if enough fluids are not given especially if the patient is vomiting so much, also watch for haematuria and oliguria. 

Complications:

for the Mother:

  • Sepsis: A severe and life-threatening condition where the infection spreads throughout the body.
  • Kidney Damage: Repeated or untreated pyelonephritis can lead to long-term damage to the kidneys, potentially causing chronic kidney disease.
  • Preterm Labor: The infection can trigger premature contractions and lead to premature birth, especially in the second and third trimesters.
  • Low Birth Weight: Pyelonephritis can restrict fetal growth, leading to babies being born with low birth weight.
  • Urinary Tract Obstruction: Infection can contribute to or worsen urinary tract blockages, making it harder to treat the infection.
  • Acute Renal Failure: In rare cases, severe pyelonephritis can lead to kidney failure, requiring dialysis.

for the Fetus:

  • Premature Birth: As mentioned above, premature delivery is a significant risk.
  • Fetal Growth Restriction: The infection can hinder fetal growth and development.
  • Stillbirth: In severe cases, pyelonephritis can increase the risk of stillbirth.
  • Congenital Anomalies: While not fully established, some studies suggest a possible link between pyelonephritis in pregnancy and certain congenital anomalies in the baby.

CYSTITIS 

Cystitis is a lower urinary infection involving inflammation of the urinary bladder. 

Acute bacterial cystitis is common in women as the short urethra predisposes them to infection of the bladder. 

It is defined as significant bacteriuria with associated bladder mucosal invasion presenting as urgency, frequency, dysuria, pyuria and haematuria without evidence of systemic illness.

Urine may be cloudy and malodorous and should be cultured. Has similar causative agents as asymptomatic bacteriuria- E.coli implicated in almost 80% of cases.

Causes of Cystitis 

  • Hormonal Changes: Pregnancy hormones, particularly oestrogen, can relax the bladder muscles and urethral sphincter, making it easier for bacteria to enter the bladder.
  • Urinary Tract Obstruction: The growing uterus can compress the ureters, the tubes that carry urine from the kidneys to the bladder, causing urine to back up and increasing the risk of infection.
  • Increased Urinary Frequency: Pregnancy often leads to increased urine frequency, which can flush out bacteria less effectively, increasing the risk of infection.
  • Immune System Suppression: The body’s immune system is naturally suppressed during pregnancy to protect the fetus. This suppression can make it easier for bacteria to grow and cause infection.
  • Changes in Urinary Flow: The growing uterus can compress the bladder, making it difficult to empty completely. This can leave residual urine in the bladder, providing a breeding ground for bacteria.
  • Sexual Activity: While not always the case, sexual activity can introduce bacteria into the urethra, increasing the risk of infection.
  • Previous UTIs: Having a history of UTIs increases the risk of developing cystitis during pregnancy.
  • Bladder Incompetence: This can happen during pregnancy due to hormonal changes, and is a major contributor to cystitis.
  • Ascending infections: This is a primary cause of cystitis, both in pregnancy and generally, due to bacteria traveling up the urinary tract.

Signs and symptoms

  1. Frequent Urination: Feel the urge to urinate more often than usual, even if you haven’t consumed much fluid. It’s common in pregnancy anyway, but the urge may be particularly strong and urgent with cystitis.
  2. Painful Urination (Dysuria): A burning or stinging sensation during urination is a hallmark symptom. This can be especially uncomfortable during pregnancy, as the bladder may be more sensitive.
  3. Urgency: A strong, sudden urge to urinate that’s difficult to ignore. This can be exacerbated by the pressure of the growing uterus on the bladder.
  4. Pelvic Pain: A dull ache or pressure in the lower abdomen or pelvis, often located above the pubic bone.
  5. Blood in Urine (Hematuria): Presence of blood in your urine, ranging from a faint pink to bright red. While rare, it can happen with cystitis and is a sign that the infection is more severe.
  6. Fever: A low-grade fever, usually below 101°F (38.3°C), may occur with cystitis.
  7. Cloudy Urine: Urine may appear cloudy or have a strong odour/smell.
  8. Nausea and Vomiting: While less common, these symptoms can occur with severe cystitis.
  9. Back Pain: If the infection has spread to the kidneys (pyelonephritis), you may experience back pain, often on one side.
  10. Chills: If you have a fever, you may also experience chills.

Management of Cystitis in Pregnancy

Assessment:

History and Physical Exam:

  • Thoroughly assess the patient’s symptoms (frequency, urgency, pain, fever, etc.).
  • Obtain a detailed medical history, including any existing conditions, previous urinary tract infections (UTIs), and current medications.
  • Perform a physical exam focusing on signs of dehydration, fever, tenderness in the abdomen or back, and a general assessment of her overall health.

Urinalysis and Urine Culture:

  • Obtain a urine sample for urinalysis and culture to confirm the presence of bacteria and identify the specific strain. This is crucial for guiding antibiotic choice.

Treatment

Hydration:

  • Encourage the patient to drink plenty of fluids, especially water, to flush out the bacteria and prevent dehydration.

Antibiotics:

Choice: The choice of antibiotic will depend on the specific organism identified in the urine culture. The following options are commonly used for UTIs during pregnancy:

  • Nitrofurantoin: A first-line option, generally safe in pregnancy, especially during the first trimester.
  • Amoxicillin/Amoxicillin-Clavulanate: Effective against many common UTI bacteria.
  • Cephalexin: Another safe and effective option.
  • Fosfomycin: A single-dose antibiotic that can be an option for uncomplicated cystitis.

Duration: The antibiotic course should be for 7 days, even if symptoms resolve sooner. This is to prevent persistent bacteriuria and recurrent UTIs.

Admission vs. Outpatient Management

Outpatient Management:

  • Most cases of uncomplicated cystitis in pregnancy can be managed as outpatients.
  • The patient can be discharged home with instructions to take the prescribed antibiotics, stay well-hydrated, and monitor for any worsening symptoms.

Admission to Hospital:

Admission may be considered in cases of:

  • Severe Symptoms: High fever, chills, nausea, vomiting, severe pain, or blood in the urine.
  • Pregnancy Complications: Premature labor, preeclampsia, or other complications.
  • Failed Outpatient Treatment: If symptoms worsen or persist despite antibiotics.
  • Underlying Conditions: If the patient has other health issues like diabetes or kidney disease.

Follow-up and Discharge:

Follow-up:

  • Schedule a follow-up visit with the patient 1-2 weeks after completing the antibiotic course. This should be negative to confirm effective treatment.
  • Repeat urinalysis and urine culture to confirm eradication of the infection.

Discharge Instructions:

  • Advise the patient to continue adequate hydration.
  • Educate her on the importance of wiping from front to back after using the toilet to reduce the risk of recurrent UTIs.
  • Explain the signs and symptoms of complications (fever, chills, severe pain) and when to seek immediate medical attention.

Nursing care plan for a patient with renal diseases in pregnancy

Assessment

Nursing Diagnosis

Goals/Expected Outcomes

Intervention

Rationale

Evaluation

Patient reports fatigue and weakness

Fatigue related to decreased erythropoietin production and anaemia secondary to renal disease as evidenced by patient reports of feeling tired and weak.

– Reduce fatigue within 48 hours.

– Patient reports improved energy levels.

– Encourage frequent rest periods.

– Administer iron supplements as prescribed.

– Educate patient on energy conservation techniques.

– Rest periods help prevent overexertion.

– Iron supplements help correct anemia.

– Energy conservation techniques help manage fatigue.

– Patient reports improved energy levels.

– Fatigue is reduced.

Blood pressure 150/100 mmHg, proteinuria, peripheral edema

Ineffective Renal Perfusion related to altered blood flow to the kidneys as evidenced by hypertension, proteinuria, and peripheral edema.

– Maintain effective renal perfusion within 24 hours.

– Blood pressure stabilized within normal range.

– Decrease in proteinuria and edema.

– Monitor blood pressure and urine output regularly.

– Administer antihypertensive medications as prescribed.

– Educate patient on the importance of medication adherence and lifestyle modifications.

– Regular monitoring detects early changes in renal perfusion.

– Antihypertensive medications help control blood pressure.

– Patient education promotes adherence to treatment.

– Blood pressure stabilized within normal range.

– Proteinuria and edema decreased.

Patient reports difficulty breathing, SpO2 88%, crackles on lung auscultation

Impaired Gas Exchange related to fluid overload secondary to renal disease as evidenced by difficulty breathing, decreased SpO2, and crackles on lung auscultation.

– Improve gas exchange within 4 hours.

– SpO2 improved to 92% or higher.

– Patient reports easier breathing.

– Administer oxygen therapy as prescribed.

– Monitor respiratory status and SpO2 regularly.

– Administer diuretics as prescribed and monitor fluid balance.

– Oxygen therapy improves oxygen saturation.

– Regular monitoring ensures timely adjustments in care.

– Diuretics help reduce fluid overload and improve breathing.

– SpO2 improved to 92% or higher.

– Patient reports easier breathing.

– Crackles on lung auscultation decreased.

Patient reports difficulty concentrating, confusion, serum creatinine elevated

Acute Confusion related to uremia secondary to renal disease as evidenced by difficulty concentrating, confusion, and elevated serum creatinine.

– Prevent acute confusion within 24 hours.

– Patient demonstrates improved cognitive function.

– Monitor neurological status regularly.

– Educate patient and family on signs of worsening renal function.

– Administer medications to manage uremia as prescribed.

– Regular monitoring detects early signs of confusion.

– Patient education promotes early intervention.

– Medications help manage uremia and prevent confusion.

– Patient demonstrates improved cognitive function.

– No signs of acute confusion.

Patient reports swelling, weight gain, decreased urine output

Fluid Volume Excess related to impaired renal function as evidenced by swelling, weight gain, and decreased urine output.

– Maintain fluid balance within 24 hours.

– Decrease in swelling and weight gain.

– Urine output normalized.

– Monitor daily weight and intake/output.

– Administer diuretics as prescribed.

– Educate patient on low-sodium diet.

– Regular monitoring helps assess fluid status.

– Diuretics help reduce fluid retention.

– Low-sodium diet prevents fluid overload.

– Swelling and weight gain decreased.

– Urine output normalized.

– Fluid balance maintained.

Renal Diseases in Pregnancy Read More »

Dracunculosis (Guinea worm)

Dracunculiasis (Guinea Worm Disease)

Dracunculiasis is a parasitic disease caused by the nematode worm Dracunculus medinensis. 

It is characterized by the emergence of a long, thread-like worm from a painful blister on the skin, usually on the legs or feet.

Dracunculiasis is a neglected tropical disease (NTD) that primarily affects poor communities in rural areas with limited access to safe water. It is a debilitating disease that can cause significant pain and disability.

The disease is transmitted through contaminated drinking water.

Transmission:

Vector: The disease is transmitted by copepods, tiny crustaceans found in stagnant water.

Lifecycle:

  • In the Copepod (Vector):
  1. Copepods ingest the infective larvae of Dracunculus medinensis from contaminated water.
  2. The larvae develop into infective stage within the copepod.
  • In Humans (Host):
  1. Humans become infected when they drink contaminated water containing the infected copepods.
  2. In the human stomach, the copepod is digested, releasing the larvae.
  3. The larvae penetrate the intestinal wall and migrate through the body, typically reaching subcutaneous tissue (beneath the skin).
  4. Larvae mature into adult worms within one year.
  5. The female worm migrates to the surface of the skin and emerges from a blister, usually on the legs or feet.
  6. The worm releases larvae into the water, continuing the cycle.

Routes of Transmission:

  • Drinking Contaminated Water: This is the primary route of transmission.

Causes/Aetiology:

  • Dracunculus medinensis Worm: The disease is caused by the Dracunculus medinensis nematode.

Clinical Features:

Initial Stage:

  • A small, itchy blister appears on the skin, typically on the legs or feet.
  • Fever, nausea, and vomiting may occur.

Blister Stage:

  • Blister becomes painful, swollen, and filled with fluid.
  • The worm may be visible within the blister.

Worm Emergence Stage:

  • The female worm emerges from the blister, forming a long, thread-like structure.
  • The worm can be several feet long and can cause intense pain as it emerges.

Secondary Complications:

  • Infection of the wound: The emergence site can become infected with bacteria.
  • Joint pain and stiffness.
  • Lymphedema: Fluid buildup in the affected limb.
  • Abscess formation: Pus collection around the worm.

Other Symptoms:

  • Swelling and tenderness of the lymph nodes.
  • Generalized weakness.
  • Loss of appetite.

Diagnosis and Investigations:

  • Clinical Examination: A typical blister with a visible worm emerging is usually diagnostic.
  • Microscopic Examination: Examining the blister fluid or the emerging worm under a microscope can confirm the presence of Dracunculus medinensis.
  • Serological Tests: Blood tests to detect antibodies against Dracunculus medinensis.

Prevention:

  • Safe Water: Provide access to safe drinking water sources and promote safe water handling practices.
  • Water Filtration: Use filters to remove copepods from drinking water.
  • Boiling Water: Boiling water for at least 1 minute kills copepods.
  • Education: Educate communities about the disease, its transmission, and prevention strategies.
  • Environmental Management: Control mosquito breeding sites and improve sanitation in rural areas.

Management:

  • There is no known drug treatment for guinea worm 

Aims of Management:

  • To relieve pain and discomfort.
  • To prevent secondary infections.
  • To prevent transmission of the disease.

Early Management:

  • Wound Care: Clean the affected area with antiseptic solutions and dress the wound.
  • Pain Relief: Administer pain relievers as needed.
  • Preventing Secondary Infections: Administer antibiotics if secondary bacterial infection is suspected.
  • Extraction of the Worm: A healthcare provider can carefully extract the worm from the blister. This process can be slow and painful and may take several days.

Medical Management:

All patients: 

  • To facilitate removal of the worm, slowly and carefully roll it onto a small stick over a period of days.
  • Dress the wound occlusively to prevent the worm passing ova into the water.
  • Give analgesics for as long as necessary If there is ulceration and secondary infection give: 
  • Amoxicillin 500 mg every 8 hours for 5 days 
  • Child: 250 mg every 8 hours for 5 days 
  • Or cloxacillin 500 mg every 6 hours for 5 days
  • Pain Relief: Over-the-counter pain relievers can help manage pain.
  • Antibiotics: Prescribed for any bacterial infections.
  • Anti-inflammatory Medications: Can help reduce swelling and inflammation.

Nursing Care:

  • Pain Management: Assist patients in managing pain and discomfort.
  • Wound Care: Provide wound care and dressing changes as needed.
  • Infection Prevention: Monitor for signs of infection and ensure appropriate wound care.
  • Education: Teach patients about the disease, treatment, and prevention strategies.

Complications:

  • Secondary Infections: The emergence site can become infected with bacteria, leading to cellulitis, abscesses, or sepsis.
  • Arthritis: The worm can migrate into joints, causing inflammation and pain.
  • Lymphedema: Fluid buildup in the affected limb due to lymphatic obstruction.
  • Disability: Chronic pain, joint stiffness, and lymphedema can lead to significant disability.
  • Social Stigma: The disease can lead to social isolation and discrimination.

Dracunculosis (Guinea worm) Read More »

Elephantiasis (Bancroftian Filariasis)

Elephantiasis (Lymphatic Filariasis)

Elephantiasis, also known as lymphatic filariasis, is a chronic parasitic disease caused by filarial worms. 

It results in severe swelling, primarily of the legs, arms, breasts, and genitals, due to blockage of the lymphatic system. The condition gets its name from the enlargement of affected limbs, resembling that of an elephant.

Elephantiasis is a debilitating disease that can significantly impact a person’s physical, social, and economic well-being. The swelling can cause pain, disfigurement, disability, and social stigma. It is a neglected tropical disease (NTD) primarily affecting impoverished communities in tropical and subtropical regions.

Transmission:

Vector: The disease is transmitted by mosquitoes, specifically species of the genera Culex, Anopheles, and Aedes.

Lifecycle:

In the Mosquito (Vector):

  • Infected mosquitoes ingest filarial larvae (microfilariae) from an infected person’s blood.
  • The microfilariae develop into mature larvae (L3 larvae) in the mosquito.
  • L3 larvae migrate to the mosquito’s mouthparts, ready for transmission.

In Humans (Host):

  • Infected mosquitoes bite humans, transmitting the L3 larvae into the bloodstream.
  • L3 larvae mature into adult worms in the lymphatic system, typically residing in lymph nodes.
  • Adult worms reproduce, releasing microfilariae into the bloodstream, which can then be ingested by mosquitoes, completing the cycle.

Routes of Transmission:

  • Mosquito Bite: The primary route of transmission is through the bite of an infected mosquito.
  • Blood Transfusion: Transmission is possible through contaminated blood transfusions, although less common.

Causes/Aetiology:

Filarial Worms: The disease is caused by three main species of filarial worms:

  • Wuchereria bancrofti (most common)
  • Brugia malayi
  • Brugia timori

Clinical Features:

1. Early Stage (Lymphangitis):

  • Fever
  • Chills
  • Pain and redness along lymphatic vessels
  • Lymphadenitis (swollen lymph nodes)

2. Subcutaneous Stage (Lymphedema):

  • Swelling in the extremities, particularly legs and arms.
  • Pitting edema (fluid retention that leaves indentations when pressed)
  • Skin thickening and roughness

3. Late Stage (Elephantiasis):

  • Massive swelling of the limbs, breasts, or genitals.
  • Thickened and deformed skin.
  • Lymphatic obstruction leading to fluid buildup.
  • Increased susceptibility to secondary infections.

4. Genital Manifestations:

  • Hydrocele (fluid accumulation in the scrotum).
  • Lymphoedema of the scrotum (scrotal elephantiasis).
  • Lymphoedema of the vulva (vulvar elephantiasis).

5. Other Complications:

  • Chylous ascites (fluid buildup in the abdomen).
  • Chylothorax (fluid buildup in the chest).
  • Chronic kidney disease.

Diagnosis and Investigations:

Clinical Examination: Characteristic swelling and history of mosquito bites in endemic areas.

Microscopic Examination:

  • Blood smear: To detect microfilariae in blood samples.
  • Lymph node aspirate: To detect microfilariae in lymph node fluid.

Serological Tests: Blood tests to detect antibodies against filarial worms.

Imaging Studies:

  • Ultrasound: To visualize the lymphatic system and detect adult worms.
  • CT scan: To evaluate the extent of lymphatic obstruction.
  • MRI: To assess the lymphatic system and surrounding tissues.

Prevention:

Vector Control:

  • Mosquito control measures, such as insecticide spraying, insecticide-treated bed nets, and source reduction (eliminating mosquito breeding sites).
  • Use of repellents.

Mass Drug Administration (MDA):

  • Regular administration of anti-filarial medications (DEC and albendazole) to prevent transmission and reduce disease burden.
  • Large scale treatment/preventive chemotherapy Give annually
  • to all population at risk, for 4-6 years
  • Ivermectin 150-200 mcg/kg plus albendazole 400 mg single dose

Health Education: Educate communities about the disease, transmission, and preventive measures.

Improved Sanitation and Hygiene: Maintain clean surroundings and reduce mosquito breeding sites.

Management:

Aims of Management:

  • To kill adult worms and prevent the spread of infection.
  • To reduce lymphatic obstruction and swelling.
  • To improve quality of life and reduce disability.

Medical Management:

  • Anti-filarial Medications: Diethylcarbamazine (DEC) and Albendazole are the primary drugs for treatment.
  1. Diethylcarbamazine (DEC)
  2. Albendazole
  3. Ivermectin (alternative medication)
  4. Combinations of these drugs may be used.

  • Antibiotics: For treating secondary bacterial infections.

  • Doxycycline 100 mg twice a day for 4-6 weeks (do not administer antiparasitic treatment during an acute attack)

  • Pain Relievers: To manage pain and inflammation.

  • Diuretics: To reduce fluid buildup.

  • Supportive Care:
  1. Elevate affected limbs.
  2. Use compression bandages.
  3. Manage pain and inflammation.
  4. Supportive treatment during an attack (bed rest, limb elevation, analgesics, cooling, hydration)

Continuous Management:

  • Long-term Anti-filarial Therapy: May be required to prevent disease progression.
  • Lymphedema Management:
  1. Regular massage.
  2. Compression therapy.
  3. Skin care and hygiene.

  • Monitoring for Complications: Regular follow-up appointments to monitor for complications, such as secondary infections and kidney damage.

Surgical Management:

  • Chronic case:  Supportive treatment: bandage during the day, elevation of affected limb at rest, analgesics and surgery (hydrocelectomy)
  • Surgery for Complications:
  1. Surgery may be required to treat complications such as hydrocele, lymphoedema, and chylous ascites.
  2. Lymphatic bypass surgery may be considered in some cases.

Nursing Care:

  • Symptom Management: Provide comfort measures for pain, swelling, and discomfort.
  • Skin Care: Promote good skin hygiene to prevent infections.
  • Compression Therapy: Apply compression bandages to reduce swelling and improve lymphatic flow.
  • Lymphedema Management: Teach patients techniques for self-management of lymphoedema.
  • Education: Educate patients about the disease, treatment, and prevention.

Complications:

  • Secondary Infections: Frequent skin infections due to impaired lymphatic drainage.
  • Lymphedema: Progressive swelling of the affected limbs, leading to disfigurement and disability.
  • Elephantiasis: Severe and permanent disfigurement and disability.
  • Hydrocele and Lymphoedema of the Genitals: Can cause pain, discomfort, and reproductive problems.
  • Chronic Kidney Disease: Fluid overload and lymphatic obstruction can strain the kidneys.
  • Social Stigma: Elephantiasis can lead to social isolation and discrimination.
  • Psychological Distress: The disease can have a significant impact on self-esteem and mental health.

Elephantiasis (Bancroftian Filariasis) Read More »

Schistosomiasis

Schistosomiasis (Snail Fever/bilharzia)

Schistosomiasis, also known as snail fever, is a parasitic disease caused by flatworms of the genus Schistosoma.

Schistosomiasis (also known as bilharzia or snail fever) is a disease of the large intestine and urinary tract caused by parasitic worms of the Schistosoma blood fluke.

It may infect the urinary tract or intestines.

Causes/Aetiology:

Schistosoma species: The disease is caused by five main species of Schistosoma:

  • S. haematobium: Causes urinary schistosomiasis.
  • S. mansoni: Causes intestinal schistosomiasis.
  • S. japonicum: Causes intestinal schistosomiasis.
  • S. intercalatum: Causes intestinal schistosomiasis.
  • S. mekongi: Causes intestinal schistosomiasis.

Snail intermediate host: Snails of specific species are essential for the parasite’s lifecycle.

Transmission:

  • Vector: The disease is transmitted through contact with contaminated freshwater, primarily by snails infected with Schistosoma parasites.
Lifecycle Schistosomiasis

Schistosomiasis  Lifecycle:

In the Snail (Intermediate Host):

  1. Schistosoma eggs released from an infected human enter freshwater, where they hatch into larvae called miracidia.
  2. Miracidia infect snails.
  3. Within the snail, the miracidia transform into cercariae, which are free-swimming larval forms.

In Humans (Definitive Host):

  1. Cercariae penetrate the skin of humans who come into contact with contaminated water.
  2. Cercariae mature into adult worms within the human body.
  3. Adult worms reside in the blood vessels of the intestines, bladder, or other organs.
  4. Female worms release eggs into the body, and these eggs are excreted in feces or urine.
  5. The cycle repeats as eggs enter freshwater and infect snails.

The lifecycle of Schistosoma worms starts with infected humans. The worms live in the blood vessels of the intestines and produce eggs that are released in feces. These eggs enter freshwater and hatch into microscopic larvae called miracidia.

Miracidia swim until they find a specific type of snail. Inside the snail, they multiply and transform into another type of larvae called cercariae. Cercariae leave the snail and swim in the water.

If a person enters this contaminated water, the cercariae can penetrate their skin. Once inside, they mature into adult worms. The cycle starts again when the worms reproduce and release eggs, which are then expelled in feces and enter the water.

Clinical Features schistosomiasis

Clinical Features:

1. Acute Schistosomiasis (Katayama Fever):

  • Fever
  • Chills
  • Headache
  • Muscle aches
  • Rash
  • Cough
  • Abdominal pain
  • Diarrhea
  • Enlarged liver and spleen

2. Chronic Schistosomiasis:

Urinary Schistosomiasis:

  • Blood in the urine (hematuria).
  • Frequent urination, especially at night (nocturia).
  • Painful urination (dysuria).
  • Bladder inflammation (cystitis).
  • In advanced cases, bladder fibrosis and cancer.

Intestinal Schistosomiasis:

  • Abdominal pain and cramping.
  • Diarrhea or constipation.
  • Blood in the stool (hematochezia).
  • Liver enlargement (hepatomegaly).
  • Splenomegaly (enlarged spleen).
  • In advanced cases, portal hypertension, ascites, and esophageal varices.

3. Other Manifestations:

  • Lung involvement (pulmonary schistosomiasis) with cough and shortness of breath.
  • Skin lesions (schistosomal dermatitis) with itching and papules.
  • Brain involvement (neurological schistosomiasis) with seizures, paralysis, and cognitive impairment.

Diagnosis and Investigations:

  • Stool and Urine Examination: Microscopic examination for eggs in stool or urine samples.
  • Serological Tests: Blood tests to detect antibodies against Schistosoma.
  • Imaging Studies:

    • Ultrasound: To visualize the liver, spleen, and other organs.

    • CT scan: To evaluate the bladder and kidneys.

    • MRI: To assess the brain and spinal cord.

  • Biopsy: Biopsy of affected organs (liver, bladder) to confirm the presence of eggs or adult worms.

Prevention:

Safe Water and Sanitation:

  • Provide access to safe drinking water and adequate sanitation facilities.
  • Promote proper waste disposal to prevent contamination of freshwater sources.

Health Education:

  • Educate communities about the disease, transmission, and prevention.
  • Encourage safe bathing and swimming practices in freshwater bodies.

Snail Control:

  • Reduce snail populations by using molluscicides (chemicals that kill snails).
  • Implement environmental interventions to modify snail habitats.

Mass Drug Administration (MDA):

  • Regularly administer praziquantel to all individuals in endemic areas to control the disease.

Management:

Aims of Management:

  • To kill adult worms and prevent egg production.
  • To treat existing symptoms and complications.
  • To prevent further transmission of the disease.

Medical Management:

  • Praziquantel: The primary drug for schistosomiasis, effective in killing both adult worms and reducing egg production.
  • Praziquantel 40 mg/kg single dose
  • Refer patient if they develop obstruction or bleeding.
  • Other Medications:
  1. Antibiotics: For treating secondary bacterial infections.
  2. Pain relievers: For managing pain and discomfort.
  3. Anti-inflammatory medications: For reducing inflammation.
  • Symptomatic Treatment: Address specific symptoms such as fever, diarrhea, and urinary problems.

Nursing Care:

  • Symptom Management: Provide comfort measures for fever, pain, and diarrhea.
  • Hydration: Encourage fluid intake to prevent dehydration.
  • Hygiene: Promote proper hygiene to prevent infection.
  • Education: Educate patients about the disease, treatment, and prevention.
  • Monitoring: Monitor for signs of complications, including liver problems, bladder dysfunction, and neurological symptoms.

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Onchocerciasis (River blindness)

Onchocerciasis (River Blindness)

Onchocerciasis, also known as river blindness, is a chronic parasitic disease caused by the nematode worm Onchocerca volvulus. 

It is characterized by severe itching, skin lesions, and, in advanced cases, blindness. The disease is primarily found in sub-Saharan Africa, with smaller outbreaks in Central and South America.

Transmission:

Vector: The disease is transmitted through the bite of infected blackflies (genus Simulium) that live near fast-flowing rivers and streams, hence the name “river blindness.”

Lifecycle:

In the Vector (Blackfly):

  1. The female blackfly ingests microfilariae (larval worms) from an infected human during a blood meal.
  2. Inside the blackfly, microfilariae develop into infective larvae.
  3. After approximately 1 to 2 weeks, the larvae mature and migrate to the mouthparts of the blackfly.

In Humans:

  1. An infected blackfly bites a human, injecting the infective larvae into the subcutaneous tissue.
  2. Larvae migrate to the skin, where they mature into adult worms within 1 to 2 years.
  3. Adult worms reside in nodules (onchocercomas) beneath the skin and produce microfilariae.
  4. Microfilariae travel throughout the body, especially to the eyes, skin, and lymph nodes.
  5. The cycle continues as blackflies ingest microfilariae from infected humans.

Clinical Features:

Skin Lesions:

  • Papular, itchy skin lesions (onchocercal dermatitis).
  • Hyperpigmented or depigmented skin patches.
  • Severe itching, leading to secondary bacterial infections.
  • “Elephantine” skin thickening, especially on the legs and scrotum.

Eye Involvement:

  • Microfilariae migrate to the eyes, causing inflammation (onchocercal keratitis).
  • Loss of vision, including blindness, due to corneal scarring, optic atrophy, and retinal detachment.
  • Severe itching and burning in the eyes.

Onchocercomas:

  • Firm, subcutaneous nodules that contain adult worms.
  • Located in various parts of the body, including the head, neck, limbs, and buttocks.
  • Often painful and can cause pressure on nearby nerves or organs.

Lymphatic Involvement:

  • Swelling of lymph nodes and lymphedema.
  • Chronic inflammation of the lymph system.

General Symptoms:

  • Fever
  • Headache
  • Fatigue
  • Joint pain
  • Loss of appetite
  • Weight loss

Diagnosis and Investigations:

  • Skin Biopsy: Examination of skin samples for microfilariae under a microscope.
  • Slit-lamp Examination: Examination of the eyes to detect microfilariae and eye damage.
  • Nodule Biopsy: Biopsy of onchocercomas to confirm the presence of adult worms.
  • ELISA (Enzyme-Linked Immunosorbent Assay): Blood test to detect antibodies against Onchocerca volvulus.

Prevention:

Vector Control:

  • Reducing blackfly populations through insecticides and larvicides.
  • Using insect repellents and protective clothing.
  • Avoiding areas with high blackfly density.

Mass Drug Administration (MDA):

  • Regular administration of antiparasitic drugs (ivermectin) to kill microfilariae.
  • Typically given every 6 months to all individuals in endemic areas.
  • Ivermectin 150 micrograms/kg once yearly for 10-14 years 

Management:

Aims of Management:

  • To eliminate microfilariae and reduce the number of adult worms.
  • To prevent further transmission of the disease.
  • To manage complications and improve quality of life.

 

Medical Management:

  • Antibiotics: For treating secondary bacterial infections.
  • Doxycycline 100 mg twice a day for 6 weeks followed by;
  • Antiparasitic Drugs:
  • Ivermectin: Kills microfilariae but does not eliminate adult worms.

    • Ivermectin 150 micrograms/kg single dose.

  • Anti-Inflammatory Medications: For managing eye inflammation and other inflammatory conditions.

Surgical Management:

  • Excision of Onchocercomas: Surgical removal of nodules can be considered for symptomatic nodules or those causing pressure on nearby structures.

Nursing Care:

Symptom Management:

  • Provide comfort measures for itching and pain.
  • Administer medications as prescribed.
  • Monitor for side effects of medications.

Eye Care:

  • Teach patients proper eye hygiene and care.
  • Monitor for signs of eye infection and vision loss.

Skin Care:

  • Provide soothing baths and lotions for itching.
  • Encourage the use of insect repellents.

Education:

  • Educate patients about the disease, transmission, and prevention.
  • Encourage adherence to treatment and follow-up appointments.

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Helminthic diseases (Intestinal worms)

Helminthiasis/Worm Infestation

Helminthiasis, commonly known as worm infestation, refers to a group of infections caused by parasitic worms living within the human body. 

These infections are widespread, particularly in tropical and subtropical regions, affecting millions of people globally. 

Helminthiasis:

Helminthiasis encompasses infections caused by parasitic worms belonging to three major groups:

1. Nematodes (roundworms): These are cylindrical, unsegmented worms with a pointed tail. Examples include 

  • Ascaris lumbricoides, hookworms (Ancylostoma caninum and Necator americanus), and Trichuris trichiura.

2. Cestodes (tapeworms): These are flat, ribbon-like worms with segments (proglottids). 

  • Taenia saginata, Taenia solium, and Diphyllobothrium latum are some commonly encountered species.

3. Trematodes (flukes): These are flat, leaf-like worms with a complex life cycle involving multiple hosts. 

  • Schistosoma species (blood flukes), Fasciola hepatica (liver fluke), and Clonorchis sinensis (Chinese liver fluke) are examples.
Lifecycles of Helminthiasis

Lifecycles of Helminthiasis

Helminthic infections occur when a host ingests or comes into contact with infectious stages of the parasite. The specific mode of transmission varies depending on the type of worm:

Transmission Routes & Lifecycle:

1. Fecal-Oral Route:

Nematodes like Ascaris lumbricoides, hookworms, and Trichuris trichiura: Human feces containing parasite eggs are released into the environment. These eggs mature and become infective. Humans become infected by ingesting contaminated soil, water, or food containing these eggs.

Lifecycle Example: Ascaris lumbricoides

  • Eggs: Ingested eggs hatch in the small intestine, releasing larvae.
  • Larvae: Larvae penetrate the intestinal wall, enter the bloodstream, and migrate to the lungs.
  • Adult Worms: Larvae mature in the lungs, migrate up the respiratory tract, are swallowed, and reach the small intestine where they mature into adults. Adult worms produce eggs that are passed in feces.

2. Skin Penetration:

Hookworms (Ancylostoma caninum and Necator americanus): Infective larvae present in contaminated soil penetrate the skin, usually through the feet.

Lifecycle Example: Hookworms

  • Larvae: Infective larvae in soil penetrate the skin.
  • Bloodstream Migration: Larvae travel through the bloodstream to the lungs, migrate up the respiratory tract, are swallowed, and reach the small intestine.
  • Adult Worms: Larvae mature into adults in the small intestine, where they attach to the intestinal wall and feed on blood. Eggs are produced and passed in feces.

3. Consumption of Undercooked Meat:

Cestodes like Taenia saginata and Taenia solium: Humans become infected by consuming undercooked meat containing the parasite’s larval stage (cysticercus).

Lifecycle Example: Taenia saginata (beef tapeworm)

  • Ingestion of Cysticercus: Humans ingest undercooked beef containing cysticerci.
  • Adult Worm: Cysticerci mature into adult tapeworms in the small intestine.
  • Eggs: Eggs are released from the adult worm and passed in feces, contaminating the environment.

4. Consumption of Raw or Undercooked Fish:

Cestodes like Diphyllobothrium latum: Humans become infected by consuming raw or undercooked fish containing the parasite’s larval stage (plerocercoid).

Lifecycle Example: Diphyllobothrium latum (broad fish tapeworm)

  • Ingestion of Plerocercoid: Humans ingest raw or undercooked fish containing plerocercoid larvae.
  • Adult Worm: Larvae mature into adult tapeworms in the small intestine.
  • Eggs: Eggs are released from the adult worm and passed in feces, contaminating the environment.
Clinical Features Helminthic diseases (Intestinal worms)

Clinical Features:

The symptoms of helminthiasis vary depending on the type of worm and the intensity of infection. Common features include:

Gastrointestinal Symptoms:

  • Abdominal pain and cramping
  • Diarrhea or constipation
  • Nausea and vomiting
  • Anorexia (loss of appetite)
  • Weight loss

Other Symptoms:

  • Fatigue and weakness
  • Anemia (caused by blood loss due to hookworms)
  • Edema (swelling)
  • Coughing (associated with larval migration in the lungs)
  • Rectal prolapse (particularly in cases of heavy Trichuris trichiura infection)
  • Skin manifestations (rash, itching)
  • Neurologic symptoms (in cases of neurocysticercosis)

Diagnosis & Investigations:

  • History and Physical Examination: Detailed information regarding symptoms, travel history, and potential exposure to contaminated environments is crucial.
  • Stool Examination: This is the primary diagnostic tool for most intestinal helminth infections. Microscopic examination of stool samples can reveal parasite eggs or larvae.
  • Blood Tests: Blood tests can help detect the presence of antibodies against specific parasitic worms (e.g., schistosomiasis).
  • Imaging Studies: Imaging techniques like X-rays, ultrasound, and MRI can be used to detect larval cysts or adult worms in certain tissues (e.g., cysticercosis).

Prevention:

Sanitation and Hygiene:

  • Proper disposal of human feces through toilets or latrines.
  • Washing hands thoroughly with soap and water after using the toilet and before preparing food.
  • Wearing shoes when walking on contaminated soil.

Safe Food Practices:

  • Washing fruits and vegetables thoroughly before consumption.
  • Cooking meat thoroughly to kill any parasitic larvae.
  • Avoiding raw or undercooked fish.

Control of Human Waste:

  • Proper disposal of human waste, including sewage treatment.
  • Education and Awareness: Public education about the risks of helminthiasis, its transmission, and prevention measures is crucial.

Management:

Aims:

  • Elimination of Parasites: The primary aim is to eliminate the parasitic worms from the body.
  • Symptomatic Relief: Addressing the symptoms associated with the infection is vital for patient comfort.
  • Prevention of Complications: Measures are taken to prevent further complications related to the infection.

Management:

  • Supportive Care: Rest, hydration, and proper nutrition are important components of initial management.
  • Anti-Emetic Medications: These can be used to alleviate nausea and vomiting.
  • Anti-Diarrheal Medications: These may be necessary to control diarrhea.
  • Pain Relief: Pain medications can be prescribed for abdominal pain.
  • Iron Supplementation: In cases of anemia caused by hookworm infection, iron supplementation is needed.
  • Anti-Helminthic Medication: Anti-helminthic medications are used to kill or expel the parasitic worms. The specific medication depends on the type of worm causing the infection.
  • Repeat Dosing: Depending on the type of worm and the intensity of infection, repeat doses of anti-helminthic medications may be necessary.

Medical Management:

Drug Therapy: Anti-helminthic medications are the mainstay of treatment for helminthiasis.

Commonly used drugs:

  • Mebendazole: Effective against roundworms (Ascaris lumbricoides, hookworms, Trichuris trichiura) and some tapeworms.
  • Albendazole: Broad-spectrum anti-helminthic agent effective against a wide range of roundworms, tapeworms, and some flukes.
  • Praziquantel: Effective against tapeworms and flukes (e.g., schistosomiasis).
  • Ivermectin: Effective against roundworms (e.g., Onchocerca volvulus, Strongyloides stercoralis) and some other parasites.

Supportive Care:

  • Iron Supplementation: In cases of anemia caused by hookworm infection, iron supplementation is needed.
  • Nutritional Support: Patients with significant weight loss may require nutritional support.
  • Fluid Management: Maintaining adequate hydration is usefu, especially for patients with diarrhea.

Infestation Type

Drug

Dosage

Roundworm, Threadworm, Hookworm, Whipworm

Albendazole

400 mg single dose (200 mg for children under 2 years)

Mebendazole

500 mg single dose (250 mg for children under 2 years)

Ivermectin

150 micrograms/kg single dose

Prevention

  • Practice proper faecal disposal.
  • Maintain personal and food hygiene.
  • Regular deworming for children every 3-6 months.
  • Avoid walking barefoot to prevent skin penetration by larvae.

Complications:

  • Intestinal Obstruction: Large numbers of adult worms (especially Ascaris lumbricoides) can obstruct the intestines, leading to severe abdominal pain, vomiting, and difficulty passing stool.
  • Malnutrition: Chronic helminthic infections can contribute to malnutrition by interfering with nutrient absorption and causing blood loss (e.g., hookworms).
  • Anemia: Hookworms can cause anemia by feeding on blood in the intestines.
  • Rectal Prolapse: Heavy infestations with Trichuris trichiura can lead to rectal prolapse.
  • Cysticercosis: Ingestion of Taenia solium eggs can lead to cysticercosis, where larval cysts develop in various tissues, including the brain.
  • Neurocysticercosis: Cysticercosis in the brain can cause seizures, headaches, and other neurological problems.
  • Schistosomiasis–related Complications: Schistosoma infection can cause liver damage, urinary tract problems, and other complications.
  • Filariasis: Filariasis, caused by parasitic worms that reside in the lymphatic system, can lead to lymphedema, elephantiasis, and other problems.

Helminthic diseases (Intestinal worms) Read More »

Trypanosomiasis (sleeping sickness)

African Trypanosomiasis (Sleeping Sickness)

Trypanosomiasis, commonly known as African trypanosomiasis or sleeping sickness, is a parasitic disease caused by protozoa of the genus Trypanosoma.

These parasites are transmitted by the tsetse fly and affect both humans and animals. The disease is endemic to sub-Saharan Africa and can be fatal if left untreated.

Aetiology:

Trypanosomiasis is caused by two main species of Trypanosoma:

  • Trypanosoma brucei rhodesiense (TBr): This species causes the acute form of the disease and is predominantly found in East and Southern Africa.
  • Trypanosoma brucei gambiense (TBg): This species causes the chronic form of the disease and is prevalent in West and Central Africa.

Life Cycle:

Vector (Tsetse Fly):

  1. Infective stage: The tsetse fly ingests trypanosomes in the metacyclic trypomastigote stage from an infected host.
  2. Multiplication: Within the fly’s gut, trypanosomes transform into procyclic trypomastigotes and multiply.
  3. Migration: The trypanosomes migrate to the salivary glands of the fly and differentiate into metacyclic trypomastigotes, the infective stage for humans and animals.
African Trypanosomiasis

Human:

  1. Infection: Metacyclic trypomastigotes are injected into the bloodstream during a fly bite.
  2. Multiplication: The trypanosomes multiply in the bloodstream as bloodstream trypomastigotes.
  3. Spread: They can cross the blood-brain barrier, reaching the CNS and transforming into meningoencephalitic trypomastigotes.

Forms of Transmission:

  • Tsetse fly: This is the primary mode of transmission. The fly acquires trypanosomes by feeding on an infected animal or human. During its subsequent feedings, it injects the parasites into the bloodstream of its new host.
  • Blood transfusion: While rare, the disease can be transmitted through contaminated blood transfusions.
  • Mother to child: Transmission from mother to child can occur during pregnancy or childbirth.

Hosts:

  • TBg: Pigs, dogs, antelopes, cows, sheep, goats, humans.
  • TBr: Antelopes, pigs, and humans (humans are the most common source of infection).

Vectors:

  • Glossina palpalis (Riverine type): Breeds along rivers and lakes and transmits mainly T. b. gambiense.
  • Glossina morsitans (Wounded type): Stays in open, lightly wooded, packed land away from water and transmits T. b. rhodesiense.

Pathogenesis:

Trypanosomiasis arises when humans or animals are infected with trypanosomes through the bite of an infected tsetse fly. The parasite enters the bloodstream and multiplies, eventually reaching the central nervous system (CNS) in the later stages of the disease.

  • Toxins: Trypanosomes produce toxins that damage tissues, causing inflammatory changes at the primary chancre, skeletal and heart muscles.
  • CNS damage: Toxins may destroy ependymal cells lining the brain ventricles, interfering with serotonin release and causing sleep disturbances.
  • Hypersensitivity reactions: The presence of trypanosomes may cause itching (pruritis) and hives (urticaria).

Clinical Presentation:

Onset: Both TBg and TBr follow a similar course, but TBr is often acute and virulent, leading to death within 2-3 years if untreated.

Stage 1: Primary/ Chancre Stage

  • History of bite
  • Local swelling/ nodule at the bite site, possibly hardened and reddened.
  • The chancre may resemble a large boil, but with less pain.
  • This stage can last 1-2 weeks and may resolve.

Stage 2: Blood Stage/ Systemic Stage/Haematolymphatic stage.

  • Fever: Intermittent fever
  • Lymphadenopathy: Swollen spleen and cervical lymph nodes (due to lymphatic spread).
  • Physical weakness: Loss of strength accompanied by fever.
  • Itchy rashes: Skin patches (15-30 cm in diameter) on the chest and back due to hypersensitivity to trypanosomes.
  • Dyspnoea: Shortness of breath due to pericardial effusion and congestive heart failure in chronic cases (TBr).
  • Hepatomegaly: Enlarged liver due to liver damage in chronic cases, with potential jaundice.
  • Pitting oedema: Swelling on the face, lower limbs, eyelids, and abdomen due to cardiac failure or kidney damage.
  • Neurological pains: Muscle cramps are common.
  • Reduced appetite and weight loss: Due to constant sleeping and difficulty eating.
  • Menstrual irregularities: Amenorrhoea in women.
  • Anaemia: Due to the destruction of red blood cells by the trypanosomes.

Stage 3: CNS Stage/ Meningoencephalitis

This stage develops after several months or years of infection, but can occur more rapidly in the acute form (TBr). It’s characterized by involvement of the central nervous system.

Sleep disturbances:

  • Daytime sleepiness, lethargy, and coma.
  • Nighttime insomnia, restlessness, and nightmares.

Behavioral changes:

  • Confusion, apathy, and disorientation.
  • Personality changes, including aggression and irritability.
  • Hallucinations and delusions.

Neurological signs:

  • Motor incoordination: Tremors, jerky movements, paralysis (facial palsy, limb weakness, difficulty swallowing), ataxia (unsteady gait).
  • Sensory disturbances: Numbness and tingling sensations.
  • Headache: Often severe and persistent.

Meningitis:

  • Stiff neck (meningismus)
  • Photophobia (sensitivity to light)
  • Fever
  • Nausea and vomiting

Other Symptoms:

  • Swelling: The face and limbs may become swollen, especially in the late stages.
  • Cardiac complications: Irregular heartbeat, heart failure, and pericarditis can occur.
  • Renal complications: Kidney failure can occur in later stages.

Diagnosis:

Clinical examination: Evaluating the patient’s history, symptoms, and neurological signs.

Laboratory investigations:

Microscopy:

  • Wet blood smear: Examination of a fresh blood sample under a microscope for the presence of trypanosomes.
  • Thick blood smear: A higher concentration of blood is used to improve detection of trypanosomes.
  • Staining: Using Giemsa or Wright’s stain to visualize the trypanosomes.

Serology: Blood tests to detect antibodies against trypanosomes.

Lumbar puncture (LP): A spinal tap to collect cerebrospinal fluid (CSF) for examination.

  • Microscopy: Examining the CSF for trypanosomes, especially in the meningoencephalitic stage.
  • Biochemical analysis: Measuring protein levels and cell counts in the CSF.

Molecular methods: PCR testing can be used to detect trypanosome DNA, especially in the early stages of infection.

Differential Diagnosis:

  • Malaria: Can present with fever, chills, sweating, and headaches.
  • Tuberculosis (TB): Can cause fever, weight loss, and night sweats.
  • Meningitis: Can cause headache, fever, stiff neck, and altered mental status.
  • HIV/AIDS: Can cause fever, weight loss, and neurological symptoms.
  • Other infections: Meningococcal meningitis, encephalitis, and viral infections.

Management:

Early Stages:

  • Suramin: Given intravenously (IV) every 3-5 days for 6-7 doses. Effective against bloodstream trypanosomes, but not CNS involvement.
  • Pentamidine: Given intramuscularly (IM) daily for 7-10 days. Effective against bloodstream trypanosomes.

Late Stages (CNS Involvement):

  • Melarsoprol (MEL.B): The only drug effective against trypanosomes in the CNS. Given intravenously and requires careful monitoring due to potential side effects.
  • Eflornithine: Alternative treatment for late-stage disease, especially in pregnant women.

Supportive Care:

  • Bed rest: To reduce the risk of complications and improve recovery.
  • Hydration: To prevent dehydration.
  • Nutrition: Adequate nutrition is essential to support the body’s fight against infection.
  • Symptom management: Medication for fever, headache, and other symptoms.

Prevention and Control:

  • Vector control: Reducing the tsetse fly population through insecticides, traps, and clearing of vegetation in endemic areas.
  • Early diagnosis and treatment: Active screening and case finding programs are crucial for timely treatment and preventing the spread of the disease.
  • Sleeping sickness awareness: Public health education about the disease, its transmission, and prevention measures.

Prognosis:

  • Untreated: The disease is almost always fatal.
  • Treated: Early treatment is important for a positive prognosis. Late-stage treatment is more challenging and has a higher risk of complications.

Nursing Management:

  • Assessment: Monitor vital signs, neurological status, and symptoms.
  • Medications: Administer medications according to the doctor’s orders and monitor for side effects.
  • Hydration: Ensure adequate fluid intake to prevent dehydration.
  • Nutrition: Provide a balanced diet to support the body’s recovery.
  • Comfort: Provide comfort measures for symptoms like fever, headache, and pain.
  • Patient education: Educate the patient and their family about the disease, its management, and preventive measures.

 

Early Stage Treatment:

Trypanosoma rhodesiense sleeping sickness:

For both children and adults: Suramin is the drug of choice for early-stage T. rhodesiense infection.

Dosage:

  • A test dose of 5 mg/kg body weight should first be administered intravenously (IV) to check for anaphylactic reactions.
  • If no reaction occurs, five injections of 20 mg/kg body weight are given every 5 days, totaling 100 mg/kg over a 23-day period.
  • The schedule is as follows:
  1. Day 0: 5 mg/kg body weight
  2. Day 3: 20 mg/kg body weight
  3. Day 8: 20 mg/kg body weight
  4. Day 13: 20 mg/kg body weight
  5. Day 18: 20 mg/kg body weight
  6. Day 23: 20 mg/kg body weight
  • Important Note: If anaphylaxis occurs after the test dose, suramin should not be administered.

Trypanosoma gambiense sleeping sickness:

  • For both children and adults: Pentamidine is the preferred treatment for early-stage T. gambiense infection.
  • Dosage: 4 mg/kg body weight daily for 7 days, administered intramuscularly (IM).
  • Important Considerations:
  • Food should be given 1 hour before pentamidine administration to prevent hypoglycemia.
  1. The patient should lie flat (supine position) during administration and for 1 hour afterward to prevent hypotension.

Late Stage Treatment:

Trypanosoma rhodesiense sleeping sickness:

  • For both children and adults: Melarsoprol is the primary treatment for late-stage T. rhodesiense infection.
  • Dosage: 2.2 mg/kg body weight daily for 10 days administered intravenously (IV).

Trypanosoma gambiense sleeping sickness:

Children ≤ 12 years and <35 kg: Eflornithine is the preferred treatment.

  • Dosage: 150 mg/kg body weight every 6 hours for 14 days (total daily dose of 600 mg/kg).
  • Administration: Dilute the 150 mg/kg dose of eflornithine in 100 ml of distilled water and administer the infusion over at least 2 hours.

Children >12 years up to 15 years: Eflornithine is the preferred treatment.

  • Dosage: 100 mg/kg body weight every 6 hours for 14 days (total daily dose of 400 mg/kg).
  • Administration: Dilute the 100 mg/kg dose of eflornithine in 100 ml of distilled water and administer the infusion over at least 2 hours (rate of 20 drops/minute).

Adults >15 years:

  • NECT (Nifurtimox/Eflornithine Combination Therapy): This is the preferred treatment for late-stage T. gambiense infection in adults.
  1. Nifurtimox dosage: 5 mg/kg body weight every 8 hours orally for 10 days (total daily dose of 15 mg/kg).
  2. Eflornithine dosage: 200 mg/kg body weight every 12 hours for 7 days (total daily dose of 400 mg/kg).
  3. Administration: Dilute the 200 mg/kg dose of eflornithine in 250 ml of distilled water and administer the infusion over at least 2 hours (rate of 50 drops/minute).

Relapses: If a relapse occurs, IV melarsoprol at 2.2 mg/kg once daily for 10 days is used.

Important Notes:

Corticosteroids:

  • Corticosteroids should be given to patients with late-stage trypanosomiasis who are receiving melarsoprol, as they may have hypoadrenalism.
  • Corticosteroids can also reduce drug reactions.
  • Hydrocortisone should not be given after day 24, even if the melarsoprol treatment is not yet complete.
  • If prednisolone is used instead of hydrocortisone, the anti-inflammatory action is similar, but the correction of hypoadrenalism will be much less effective.

Suramin:

  • Suramin should not be used for early or late-stage T. gambiense treatment in areas where onchocerciasis (river blindness) is endemic, as it can cause blindness in individuals infected with onchocerciasis by killing the filariae in the eye.

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