Weekly Tidbits 8/26-27

  1. Hepatorenal Syndrome

Type 1 HRS is characterized by rapid and progressive renal impairment and is most commonly precipitated by spontaneous bacterial peritonitis (SBP).  Type 1 HRS occurs in approximately 25% of patients with SBP, despite rapid resolution of the infection with antibiotics.  Without treatment, the median survival of patients with type 1 HRS is < 2 weeks, and virtually all patients die within 10 weeks after the onset of renal failure.

Type 2 HRS is characterized by a moderate and stable reduction in the GFR and commonly occurs in patients with relatively preserved hepatic function.  These patients are often diuretic resistant with a median survival of 3-6 months.  Although this is markedly longer than type 1 HRS, it is still shorter compared to patients with cirrhosis and ascites who do not have renal failure.

 

 

 

ATACH-II trial: What is the optimal blood pressure control for ICH patients?

Qureshi A, et al. "Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage". The New England Journal of Medicine. 2016. 
In patients with spontaneous intra-cranial hemorrhage with volume of < 60 cm3 and a Glasgow Coma Scale (GCS) score of >4/15, there is no differences in mortality or morbidity in patients receiving intensive blood pressure control (<140) compared to standard blood pressure control (140-180). 

 

Further Reading: 

Blood Pressure Goals in Intracerebral Hemorrhage – ATACH II

http://www.medscape.com/viewarticle/863450?src=trendmd_pilot

Status Epilepticus

Lung Cancer Immunology Therapy: Anti-PD-1 / PD-1 Antibodies

2017 Systemic Approaches to Advance Cancer:

1. Chemotherapy

2. Molecular targets approach (Ex: EGFR Tyrosine Kinase Inhibitors)

3. Immune Checkpoint Strategies (Ex: Anti PD-1/PD-L 1 Ab)

 

Acetaminophen Hepatotoxicity

Stage 1 (0-24hrs)

  • asymptomatic or GI upset only

Stage 2 (24-48 hrs)

  • resolution or nausea and vomiting
  • RUQ pain and tenderness
  • progressive elevation of transaminases, bilirubin, PT

Stage 3 (48-96 hrs)

  • hepatic failure (jaundice, coagulopathy, encephalopathy)

Stage 4

  • death from hepatic failure
  • normalization of LFT’s and complete resolution of hepatic architecture by 3 months

Treatment

Specific

  • decrease absorption: activated charcoal if presented within 4 hours (controversial as if NAC given then this is a benign OD)
  • N-acetyl cysteine in D5W (based on 4 hour level or empirically if > 8 hours since OD):
    -> 150mg/kg LD
    -> 50mg/kg over 4 hours
    -> 100mg/kg over 16 hours
  • can be administered at any time of presentation (up to 72 hours post ingestion with some improvement in outcome)
  • can be administered orally but efficacy reduced by 40% if given with activated charcoal
  • provides a substrate of glutathione and acts as an alternative substrate for NAPQI metabolism via the cytochrome P450 pathway
  • watch for adverse effects: rash, bronchospasm, hypotension, angioedema (antihistamines helpful and also slowing of infusion)

Liver failure management

  • don’t correct coagulopathy unless bleeding (vitamin K IV, blood products)
  • arterial ammonia (aids in prognostication: absolute level and failure to fall)
  • glucose monitoring
  • avoid hypothermia
  • reverse jugular venous saturation monitoring
  • ICP monitoring (controversial)
  • avoid hyponatraemia
  • ventilate to normocapnia
  • thiopentone and indomethacin infusions (consult with liver unit)
  • renal failure management
  • MARS therapy: some benefit shown in paracetamol OD as a bridge to transplantation