Jaundice, ascites, and encephalopathy Flashcards

Question

Prognostication with ascites

Answer 1

- Usually an indicator of advanced disease In ovarian CA, longer mean survival from the time of development when compared to other cancers as it comes on with relatively early stage CA and can be treated with chemo

Answer 2

- Intra abdo pressure - Abdominal discomfort - Dyspnea - Anorexia - Reflux - Poor mobility - Insomnia due to discomfort - N/V - Early satiety - Impacts on body image

Answer 3

Transudative (Cirrhosis, Budd-Chiari, hepatic tumours) - Portal hypertension - Results in increased venous pressure with fluid leaking into the peritoneum, with renin secretion by the kidneys and sodium/fluid retention Exudative - Peritoneal tumour bed is vascular with high permeability - Normal microvessels may become more permeable due to the malignancy driving production of inflammatory cytokines Differentiate using SAAG (serum albumin) - (ascitic albumin). If > 11, due to portal hypertension (cirrhosis, heart failure, budd chiari, etc.) and more likely to be diuretic responsive If < 11, exudative (peritoneal malignancy, TB, pancreatitis, etc.)

Answer 4

Differentiate transudative vs exudative ascites using SAAG (serum albumin) - (ascitic albumin). If > 11, due to portal hypertension (cirrhosis, heart failure, budd chiari, etc.) and more likely to be diuretic responsive If < 11, exudative (peritoneal malignancy, TB, pancreatitis, etc.)

Answer 5

Complication of retroperitoneal tumour spread or its treatment Occurs due to damage to lymphatic vessels or obstruction of lymphatic flow through lymph nodes or the pancreas

Answer 6

Physical exam When in doubt, US can detect as little as 100 ml of ascitic fluid

Answer 7

- Always exclude other potential causes (e.g. CHF, cirrhosis, nephrotic syndrome, TB, pancreatitis) 1. Cytotoxic therapy - Consider specific antitumour therapy, especially in patients with known ovarian or breast CA that may benefit greatly - Chylous ascites may benefit from chemo as well 2. Diuretic therapy - Consider a trial if the SAAG is high or patient has portal HTN, though the role of diuretics in malignant ascites is controversial - Treat with mineralocorticoid receptor antagonist with Loop (e.g. spironolactone 100mg PO qdaily + 40mg Lasix. Maintain ratio and titrate upwards. Note that this can trigger HE in patients with limited residual hepatic function!

Answer 8

- Provides quick symptomatic relief and may bridge patients to effective relief from diuretics - As per cochrane review, no evidence for speficic methods around length of time to keep the drain in place, use of albumin, clamping, or vitals after drainage. For frail patients, remove `1-2 L over 30 mins (most significant symptom relief with first 1-2 L). Otherwise, patients can often tolerate up to 5 L without issue.

Answer 9

- No peripheral edema - High SAAG (transudative) but not responding to diuretics If hypotension develops, can consider IV infusion of albumin

Answer 10

- Patients with malignant ascites not undergoing any type of cytotoxic therapy (likely to reaccumulate within a few days) - Allows repeated paracentesis from home.

Answer 11

- Bowel perforation - Peritonitis - Localised cellulitis - Leakage - Electrolyte shifts - Bleeding - Risk of hepatic failure and encephalopathy if severe hepatic compromise Anecdotally: - fatigue - hyponatremia and hypoalbuminemia over time

Answer 12

- Shunt designed to allow drainage of ascites into the central venous system through the internal jugular or femoral veins - Placed surgically, laparoscopically, or percutaneously Risks: - shunt occlusion - DIC - fluid overload - VTE - tumour seeding (though not felt to be clinically significant) Contraindications: - hemorrhagic ascites - High ascitic protein content - loculated ascites - portal HTN - renal or cardiac failure - bleeding disorder Best outcomes appear to be in patients with normal renal function and tumours of non-GI primary origin May be worth considering in patients with gyne malignancies given long survival

Answer 13

- Neuropsych disturbance as a consequence of progressive liver disease with cirrhosis - Characterised by abnormal cognitive and motor function as well as psychiatric disturbances May be due to chronic liver disease or in some cases, malignancy with massive infiltration by a primary or metastatic tumour (though usually the prognosis is in the range of days) - Sign of decompensation and related to the development of significant portosystemic venous shunting (through collateral or TIPS procedure) or damaged hepatocytes unable to metabolise ammonia Prognosis is significantly worse after first episode of acute encephalopathy in CLD and shoulkd trigger transplant w/u

Answer 14

- Ammonia build up (generated in small intestine by bacterial activity) - Normally transported by the portal vein to the liver where it is metabolised and excreted - Impaired due to either portosystemic shunting (collaterals) or hepatocyte dysfunction - Ammonia, rather than be excreted, then accumulates in the systemic circulation and cross the blood brain barrier - Results in increased GABA activity and cerebral edema due to osmotic pressure in astrocytes

Answer 15

- EtOH - Infection - Sedating drus - Dehydration - Constipation - Anemia - GI bleeding

Answer 16

- Diagnosis of exclusion - Rule out CVA and space-occupying brain lesion - Check for other causes of metabolic encephalopathy (uremia, etc.) - Worth getting a blood ammonia level Clinical signs: - Fetor hepaticus - Asterixis - Jaundice - Extrapyramidal signs (tremor, bradykinesia, cog wheel rigidity, shuffling gait)

Answer 17

Stage 0 - Impairment only noted on psychomotor testing - No asterixis Stage I - Mild lack of awareness and shortened attention span - Altered sleep pattern - Mild asterixis or tremor Stage 2 - Lethargy, disorientation, inappropriate behaviour - Slurred speech - Obvious asterixis Stage 3 - Somnolent but rousable - Disorientation - Bizarre behaviour - Asterixis absent, high muscle tone and hyperreflexia Stage 4 - Coma - Decerebrate posturing

Answer 18

1. Diet - High protein diet may in the short term worsen HE, but in the long term protein restriction can aggravate ascites and worse catabolism - Optimally, diet with vegetable protein - Consider referral to nutrition 2. Disaccharides - Lactulose will be preferentially consumed by intestinal bacteria, competitively reducing ammonia production. Also increases frequency of BMs and excretion of potential toxins - Titrate dose to target 2-3 BMs per day - Weak evidence as per cochrane 3. Antibiotics - Rifaximin to reduce urease-producing bacteria in the gut - Poorly absorbed PO and demonstrates effective reduction in ammonia - Used if HE is inadequately managed with lactulose (in addition to lactulose) 4. Ensure euvolemia as dehdration may compound the issue.

Answer 19

1. Identify and treat underlying cause - Tap for SBP, CBC, lytes, ammonia, Cr, CT head for other causes, CXR for PNA, pan culture - Check recent meds, any intoxication - History for GI bleeding, constipation 2. Lower blood ammonia - Start lactulose and titrate to 2-3 BMs per day - In unconscious patient, may need to do lactulose enemas 3. If no improvement in 48 hrs, start rifaximin PO (in addition to lactulose)