clinical scenarios 3 Flashcards

Question

How is hepatic encephalopathy graded?

Answer 1

Grade 1 – Insomnia/reversal of day/night sleep pattern Grade 2 – Lethargy/disorientation Grade 3 – Confusion Grade 4 - Coma Asterixis may be present at any stage.

Answer 2

The aim of treatment is to improve morbidity Exclude other causes of confusion Identify and correct the precipitating cause Give lactulose. This alters faecal pH and nitrogen utilisation by bowel flora. Phosphate enemas help to purge the large bowel.

Answer 3

Lactulose acidifies the gastrointestinal tract, which reduces the amount of ammonia produced by bacteria

Answer 4

Treat underlying cause - stop drinking, antiviral in viral hepatitis and immune suppression in autoimmune hepatitis Abstinence from alcohol improves prognosis in viral hepatitis and chronic liver disease. 6 monthly abdominal USS and AFP to monitor for hepatoma All patients should undergo endoscopy as surveillance for oesophageal varices Following an episode of spontaneous bacterial peritonitis, prophylactic antibiotics are indicated.

Answer 5

A transplant centre should take this decision. The selection for transplantation is taken based on the severity of the underlying liver disease against the presence of any co-morbidities. Some conditions should be considered for transplant irrespective of disease severity such as PBC or recurrent cholangitis in PSC.

Answer 6

Precipitating factors infection e.g. spontaneous bacterial peritonitis GI bleed post transjugular intrahepatic portosystemic shunt constipation drugs: sedatives, diuretics hypokalaemia renal failure increased dietary protein (uncommon)

Answer 7

Features confusion, altered GCS (see below) asterixis: 'liver flap', arrhythmic negative myoclonus with a frequency of 3-5 Hz constructional apraxia: inability to draw a 5-pointed star triphasic slow waves on EEG raised ammonia level (not commonly measured anymore)

Answer 8

Wernicke's encephalopathy is a neuropsychiatric disorder caused by thiamine deficiency which is most commonly seen in alcoholics. Rarer causes include persistent vomiting, aոοrеxiа nervosa, stomach cancer, and dietary deficiency.

Answer 9

A classic triad of ophthalmoplegia/nystagmus, ataxia and encephalopathy may occur. Features oculomotor dysfunction nystagmus (the most common ocular sign) ophthalmoplegia: lateral rectus palsy, conjugate gaze palsy gait ataxia encephalopathy: confusion, disorientation, indifference, and inattentiveness peripheral sensory neuropathy

Answer 10

If not treated Korsakoff's syndrome may develop as well. This is termed Wernicke-Korsakoff syndrome and is characterised by the addition of antero- and retrograde amnesia and confabulation in addition to the above symptoms.

Answer 11

Delirium Tremens - DT occurs in a similar population as WE and is associated with rapid onset confusion, shaking which may be confused with ataxia, and tachycardia. DT is associated with hyperthermia rather than hypothermia, however, and is usually associated with a history of having significantly reduced alcohol intake in the prior 5 days. High doses of parenteral thiamine are rapidly administered to both DT and WE patients so precise discrimination is not always required. Hepatic Encephalopathy Stroke Normal Pressure Hyrdocephalus - Normal-pressure hydrocephalus presents with Hakim's triad of mental state changes, gait instability and urinary incontinence, highly similar to the triad of mental state changes, ataxia and ocular movement abnormalities associated with WE.

Answer 12

Overview marked memory disorder often seen in alcoholics thiamine deficiency causes damage and haemorrhage to the mammillary bodies of the hypothalamus and the medial thalamus in often follows on from untreated Wernicke's encephalopathy Features anterograde amnesia: inability to acquire new memories retrograde amnesia confabulation

Answer 13

seconds to minutes – Acute asthma attack, anaphylaxis, Pneumothorax (+ Tension), Inhaled foreign body, Pulmonary Embolism Hours to Days – Pneumonia, Heart Failure, Pleural Effusion Weeks to Months – Worsening COPD, Chronic Asthma, Heart Failure, Pulmonary Fibrosis, Anaemia, Pulmonary HTN, Obesity.

Answer 14

Time and Onset Alleviating or aggravating factors - worse when lying flat , worse of exertion associated features - cough, wheeze, chest pain, pleuritic pain? weight loss or night sweats PMH and drug history any recent changes to drugs Any Allergies Have they been admitted to hospital before , have they ever been admitted to ITU Do they smoke Occupational History

Answer 15

Bedside - observations, peak flow, ECG, ABG Bloods - FBC, U&E's CRP CXR

Answer 16

State the patient is having SEVERE asthma attack if not able to finish sentences - sit the patient up in bed - high flow oxygen - salbutamol nebulisers - these can be given back to back - Steroid - IV or oral - Add nebulised ipratropium if response to beta 2 agonist is poor - monitor patient with serial peak flows before and after nebuliser. Repeat ABG if no improvement - IV abx if signs of infection - IV fluid resuscitation - IV magnesium sulphate if no response - IV aminopylline - best to get support before dong this - of making no progress - get urgent support 2222 or ITU

Answer 17

Explain that acute asthma attacks can be split into acute severe asthma and life-threatening asthma. The markers for a life-threatening asthma attack include: PEF <33% best or predicted Soft breath sounds or silent chest Feeble respiratory effort Exhaustion, drowsiness, decreasing GCS Hypotension SBP <100 Arrhythmia – suggest haemodynamic compromise Signs of cyanosis Hypoxia SpO2 <90% or PaO2 <8kPa despite 60% FiO2 Rising PaCO2 – this is the most important as it indicates ‘near-fatal’ asthma Any of these signs would prompt me to put out an arrest call as they all suggest the patient is approaching respiratory arrest

Answer 18

Initially managed on a short course of steroid They can be safely discharged once they are off of regular nebulisers and PEF is >75% of best. The patient should be started on an inhaled Corticosteroid (if not on one already). This dose should be titrated up to response. A short acting Beta-2 agonist is required for symptomatic control. A long acting Beta-2 agonist can be added following an observed response to the inhaled corticosteroid. Patient education is always important prior to discharge and should include observation of inhaler technique and PEF record keeping. Follow up arranged with GP smoking Cessation