Understanding Neurological Disorders Caused by Medications

Neurological disorders can be caused by certain medications, such as high-potency anti-psychotic drugs like haloperidol. One such disorder is neuroleptic malignant syndrome, which can result from the use of these medications to treat conditions like schizophrenia. Symptoms include muscular rigidity, fever, and altered mental status. Treatment involves discontinuing the medication and managing symptoms with cooling measures and medications like dantrolene or bromocriptine.

Another medication-induced neurological disorder is serotonin syndrome, which can occur when a patient takes multiple doses or an overdose of medications like selective serotonin reuptake inhibitors (SSRIs) or serotonin agonists. Symptoms include muscular twitching, agitation, and autonomic instability. Treatment involves discontinuing the medication and managing symptoms with supportive care.

Malignant hyperthermia is a similar disorder that can occur during anesthesia administration and is caused by an inherited genetic disorder. Symptoms include fever, muscle rigidity, and altered mental status. Treatment involves using medications like dantrolene and providing supportive care.

It’s important to note that not all neurological disorders are caused by medications. Meningitis, for example, is not a side effect of haloperidol. Acute dystonia, which presents with spasms of various muscle groups, can also be caused by haloperidol, but the presenting symptoms are more consistent with neuroleptic malignant syndrome. Understanding the different neurological disorders caused by medications can help healthcare providers make accurate diagnoses and provide appropriate treatment.

Differential Diagnosis for a Patient with Pulmonary Oedema

The patient in question is likely suffering from flash pulmonary oedema, which can be caused by mitral valve regurgitation due to mitral valve disease. This is supported by the patient’s advanced age, hypertension, hyperlipidaemia, and the presence of a new systolic murmur at the apex. The backup of blood into the left atrium and pulmonary vasculature can lead to transudation of fluid into the pulmonary alveolar space, causing pulmonary oedema.

While pericardial effusion could also lead to pulmonary congestion, it would likely manifest with Beck’s triad of distant heart sounds, hypotension, and distended neck veins. Pleural effusion, on the other hand, would result in quieter sounds on auscultation and dullness to percussion. Lobar pneumonia would be accompanied by a fever and crackles on auscultation, but would not explain the new systolic murmur. Finally, left ventricular outflow tract obstruction, such as aortic stenosis, would cause a different type of murmur at the right upper sternal border, which is not present in this case.

Differential diagnosis of hearing loss and tinnitus

Gentamicin-induced ototoxicity

A patient presenting with bilateral tinnitus and hearing loss after recent use of gentamicin is likely experiencing ototoxicity from this antibiotic. Gentamicin can damage the vestibular system and cause sensorineural hearing loss.

Bacteraemia and viral labyrinthitis

Bacteraemia, especially from methicillin-resistant S. aureus, would not cause tinnitus. Viral labyrinthitis may cause tinnitus, but it is usually accompanied by severe vertigo and hearing loss.

Hyperlipidaemia and noise-induced hearing loss

Hyperlipidaemia, particularly hypertriglyceridaemia, has been linked to an increased risk of noise-induced hearing loss and tinnitus. A low-cholesterol diet and atorvastatin may help alleviate these symptoms.

Ménière’s disease and betahistine

Ménière’s disease is a disorder of the inner ear characterized by excess endolymph, leading to severe vertigo, hearing loss, and tinnitus. Betahistine is a medication used to manage the symptoms of Ménière’s disease, but there is no cure for this condition.

Otosclerosis and conductive hearing loss

Otosclerosis is a condition that affects the bony ossicles of the ear, leading to conductive hearing loss. It results from abnormal sclerosis of the malleus, incus, and stapes, which are crucial for sound conduction from the outer to the inner ear.

If a cervical cancer screening sample is positive for high-risk strains of human papillomavirus (hrHPV) but shows no cytological abnormalities, the recommended course of action is to repeat the smear after 12 months. This is in accordance with current guidance. Colposcopy is not necessary in this case. Repeating the smear after 3 months or waiting 3 years for routine recall are also not appropriate. A repeat smear after 6 months would only be necessary after treatment for cervical intraepithelial neoplasia.

The cervical cancer screening program has evolved to include HPV testing, which allows for further risk stratification. A negative hrHPV result means a return to normal recall, while a positive result requires cytological examination. Abnormal cytology results lead to colposcopy, while normal cytology results require a repeat test at 12 months. Inadequate samples require a repeat within 3 months, and two consecutive inadequate samples lead to colposcopy. Treatment for CIN typically involves LLETZ or cryotherapy. Individuals who have been treated for CIN should be invited for a test of cure repeat cervical sample 6 months after treatment.

Cardiac Abnormalities and their Clinical Findings

Atrial Septal Defect:
Atrial septal defect is characterized by a prominent right ventricular cardiac impulse, a systolic ejection murmur heard best in the pulmonic area and along the left sternal border, and fixed splitting of the second heart sound. These findings are due to an abnormal left-to-right shunt through the defect, which creates a volume overload on the right side. Small atrial septal defects are usually asymptomatic.

Pulmonary Valve Stenosis:
Pulmonary valve stenosis causes an increased right ventricular pressure which results in right ventricular hypertrophy and pulmonary artery dilation. A crescendo–decrescendo murmur may be heard if there is a severe stenosis. Right atrial enlargement would not be present.

Mitral Regurgitation:
Mitral regurgitation would also present with a systolic murmur; however, left atrial enlargement would be seen before right ventricular enlargement.

Mitral Stenosis:
Mitral stenosis would present with an ‘opening snap’ and a diastolic murmur.

Aortic Stenosis:
Aortic stenosis is also associated with a systolic ejection murmur. However, the murmur is usually loudest at the right sternal border and radiates upwards to the jugular notch. Aortic stenosis is associated with left ventricular hypertrophy.

Clinical Findings of Common Cardiac Abnormalities

Avascular Necrosis and Its Causes

Avascular necrosis (AVN) is a condition that occurs when the blood supply to the bones is temporarily or permanently lost. This can be caused by various factors, including trauma or vascular disease. Some of the conditions that can lead to AVN include hypertension, sickle cell disease, caisson disease, and radiation-induced arthritis. Additionally, certain factors such as corticosteroid therapy, connective tissue disease, alcohol abuse, marrow storage disease (Gaucher’s disease), and dyslipoproteinaemia can also be associated with AVN in a more complex manner.

Of all the cases of non-traumatic avascular necrosis, 35% are associated with systemic (oral or intravenous) corticosteroid use. It is important to understand the causes of AVN in order to prevent and manage the condition effectively. By identifying the underlying factors that contribute to AVN, healthcare professionals can develop appropriate treatment plans and help patients manage their symptoms. With proper care and management, individuals with AVN can lead healthy and fulfilling lives.

Rapidly Unwell Patient on Haemodialysis: Consider Line Infection

When a patient who was previously healthy becomes rapidly unwell after starting haemodialysis, it is crucial to consider the possibility of a line infection. Symptoms may include low blood pressure, sweating, and a fever. Although haemodialysis lines are silver-coated to reduce the risk of infection, line infection remains a significant problem. During haemodialysis, blood is returned to the patient through the infected line, causing a rapid bacteraemia and systemic inflammatory response that can lead to a sudden drop in blood pressure.

While other conditions such as urinary tract or lower respiratory tract infections and perforated diverticulum are possible, they are less likely to present as rapidly as a line infection. Patients with end-stage renal failure are at higher risk of cardiovascular disease, including myocardial infarction, but chest pain that develops after a drop in blood pressure may indicate a secondary rather than primary cause. Although a fever is more suggestive of infection, it is important to obtain an ECG and check for signs of myocardial infarction. In summary, when a patient on haemodialysis becomes rapidly unwell, line infection should be considered as a potential cause.

According to RCOG guidelines, women typically feel fetal movements by 20 weeks of gestation. However, if no movements are felt by 24 weeks, it is recommended to refer the woman to a maternal fetal medicine unit to assess for potential neuromuscular conditions.

Understanding Reduced Fetal Movements

Introduction:
Reduced fetal movements can indicate fetal distress and are a response to chronic hypoxia in utero. This can lead to stillbirth and fetal growth restriction. It is believed that placental insufficiency may also be linked to reduced fetal movements.

Physiology:
Quickening is the first onset of fetal movements, which usually occurs between 18-20 weeks gestation and increases until 32 weeks gestation. Multiparous women may experience fetal movements sooner. Fetal movements should not reduce towards the end of pregnancy. There is no established definition for what constitutes reduced fetal movements, but less than 10 movements within 2 hours (in pregnancies past 28 weeks gestation) is an indication for further assessment.

Epidemiology:
Reduced fetal movements affect up to 15% of pregnancies, with 3-5% of pregnant women having recurrent presentations with RFM. Fetal movements should be established by 24 weeks gestation.

Risk factors for reduced fetal movements:
Posture, distraction, placental position, medication, fetal position, body habitus, amniotic fluid volume, and fetal size can all affect fetal movement awareness.

Investigations:
Fetal movements are usually based on maternal perception, but can also be objectively assessed using handheld Doppler or ultrasonography. Investigations are dependent on gestation at onset of RFM. If concern remains, despite normal CTG, urgent (within 24 hours) ultrasound can be used.

Prognosis:
Reduced fetal movements can represent fetal distress, but in 70% of pregnancies with a single episode of reduced fetal movement, there is no onward complication. However, between 40-55% of women who suffer from stillbirth experience reduced fetal movements prior to diagnosis. Recurrent RFM requires further investigations to consider structural or genetic fetal abnormalities.

Management of Anaphylaxis: Initial Treatment and Beyond

Anaphylaxis is a life-threatening condition that requires prompt and appropriate management. The Resuscitation Council has established three criteria for diagnosing anaphylaxis: sudden onset and rapid progression of symptoms, life-threatening airway, breathing, and circulatory problems, and skin changes. The initial management for anaphylaxis is IM 1 : 1000 adrenaline 500 micrograms, even before equipment or IV access is available. Once expertise and equipment are available, the airway should be stabilized, high-flow oxygen given, the patient fluid-challenged, and IV hydrocortisone and chlorphenamine given. Ephedrine has no role in anaphylaxis, and IV adrenaline is not the first-line management. Prompt intubation may be necessary, but IM adrenaline must be given before a full ABCDE assessment is made. Nebulized adrenaline may help with airway swelling, but it will not treat the underlying immunological phenomenon. Proper management of anaphylaxis requires a comprehensive approach that addresses both the immediate and long-term needs of the patient.

Common Inducing Anaesthetic Agents and Their Uses

Propofol, etomidate, ketamine, midazolam, and thiopental are all commonly used inducing anaesthetic agents with varying properties and uses.

Propofol is the drug of choice for RSII procedures in normotensive individuals without obvious cardiovascular pathology. It has amnesic, anxiolytic, anticonvulsant, and muscle relaxant properties, but no analgesic effects.

Etomidate provides haemodynamic stability without histamine activity and minimal analgesic effects. It is used in RSI procedures in patients with raised intracranial pressure and cardiovascular conditions, often in combination with fentanyl.

Ketamine is a non-competitive glutamate N-methyl-D-aspartate (NMDA) receptor blocker that produces dissociative anaesthesia. It can be used for induction of anaesthesia in patients with hypotension, status asthmaticus, and shock, but is avoided in hypertensive patients due to relative contraindications.

Midazolam is a benzodiazepine with anticonvulsive, muscle relaxant, and anaesthetic actions. At higher doses or in combination with other opioids, it induces significant cardiovascular and respiratory depression.

Thiopental is administered intravenously as an inducing anaesthetic agent or as a short-acting anaesthetic. It is also used as an anticonvulsant agent and to decrease intracranial pressure in neurosurgical procedures.