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52 yo Male brought in by a caretaker to the ED
CC: Generalized weakness, poor appetite and jaundice.
- Brought in by his caretaker/daughter
- Lethargic
- Severe abdominal distension without pain
- At least a 'box' of wine a day for the past year
- No SOB, NVD, or fever
HTN
GERD
Paroxysmal A fib
OSA
Varicose veins of bilateral LE
Alcohol abuse
Medications
Gabapentin 300 mg PRN
Losartan 50 mg QHS
Sotalol 80 mg BID
Positive for: -
Fatigue
Shortness of breath
Generalized weakness
Labs
Alk phos 392
AST/ALT 606/171
T bili 11.4
Direct bili 9
Infectious workup negative
Lactate 4.0 >> 5.3 (after 3 hours)
US abdomen
Hepatomegaly with steatosis, no convincing intrahepatic dilatation.
Acute on chronic alcohol intoxication/withdrawal
- CIWA
- GI consult
- PPI
Dehydration
- IV fluids
Elevated LFTs, secondary to ETOH abuse
- Trending down (???)
Generalized weakness
- PT/OT
Iron deficiency
- oral supplement when awake
(She decided to intubate the patient and transfer him to RPH.)
1. Vent dependent respiratory failure
... turns out the patient was on precedex
X-ray - possible aspiration
- Empiric Abx broadened to Zosyn and vanco.
2. Metabolic encephalopathy
Infectious vs. possible liver failure.
Urgent GI consult
3. Sinus tachycardia with elevated D-dimer
- high risk for PE, on Lovenox
- CTA chest pending
4. Acute hepatitis superimposed on alcoholic cirrhosis
- Liver enzymes down but Tbili trending up.
Acute on chronic alcoholic hepatitis
Prednisolone 40 mg daily
CIWA
GI
PPI
Zosyn
AKI
Baseline Cr 0.6-0.9, p/w 1.3
UTI/Cystitis
Suspected psoas hemorrhage
Possible PE
Warrants a study of two topics.
The decline in kidney perfusion in this setting is associated with
- reductions in glomerular filtration rate (GFR)
- sodium excretion (often to less than 10 mEq/day in advanced cirrhosis)
- a fall in mean arterial pressure
Splanchnic vasodilatation = Significant.
Proved by response to ornipressin, an analog of antidiuretic hormone (arginine vasopressin)
= A preferential splanchnic vasoconstrictor
HRS-AKI (type 1)
- x 2 increase in serum Cr. (i.e. 50% reduction in CrCl) within 2 weeks
- May be oliguric
Diuretic-resistant ascites (type 2)
- Ascites resistant to diuretics
- less serious than type 1
A prospective study from 2011
562 patients with cirrhosis and kidney function impairment
● Kidney injury associated with infection (e.g. sepsis or spontaneous bacterial peritonitis) – 46 %
● Prerenal acute kidney injury – 32 %
● Hepatorenal syndrome – 13 %
● Parenchymal kidney disease (such as glomerulonephritis) – 9 %
- Stop antihypertensive agents, including beta-blockers
- If in ICU, use norepinephrine + albumin. (Norepinephrine 0.5 - 3 mg/hr, to raise the MAP by 10 mmHg. Albumin for 2 days, 1g/kg per day, 100g = max)
IV vasopressin may also be effective
- If NOT in ICU, terlipressin (IV, 1-2mg Q4-6H) + albumin.
If terlipressin NOT available, midodrine, octreotide and albumin.
- If medical Tx fails, Transjugular Intrahepatic Portosystemic Shunt... too many complications.
- Or... DIALYSIS and then transplant.
El Chediak, A., Janom, K. & Koubar, S.H. Bile cast nephropathy: when the kidneys turn yellow. Ren Replace Ther 6, 15 (2020). https://doi.org/10.1186/s41100-020-00265-0
Patel, J., Walayat, S., Kalva, N., Palmer-Hill, S., & Dhillon, S. (2016). Bile cast nephropathy: A case report and review of the literature. World Journal of Gastroenterology, 22(27), 6328.
Van Slambrouck, C. M., Salem, F., Meehan, S. M., & Chang, A. (2013). Bile cast nephropathy is a common pathologic finding for kidney injury associated with severe liver dysfunction. Kidney international, 84(1), 192-197.
Soman, S., Aurora, L. (2021). Type 3 Cardiorenal Syndrome. In: McCullough, P.A., Ronco, C. (eds) Textbook of Cardiorenal Medicine. Springer, Cham. https://doi.org/10.1007/978-3-030-57460-4_9
https://healthjade.net/portal-vein/
https://www.uptodate.com/contents/hepatorenal-syndrome?search=hepatorenal%20syndrome&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
Stocker, R., Yamamoto, Y., McDonagh, A. F., Glazer, A. N., & Ames, B. N. (1987). Bilirubin is an antioxidant of possible physiological importance. Science, 235(4792), 1043-1046.
https://www.microscopyu.com/techniques/polarized-light/principles-of-birefringence
Ziberna, L., Martelanc, M., Franko, M., & Passamonti, S. (2016). Bilirubin is an endogenous antioxidant in human vascular endothelial cells. Scientific reports, 6(1), 1-6.
AKI on CKD III
Etiology:
- Prerenal
- Possible hepatorenal
- Contrast-induced
- Bilirubin induced ATN
AKI on CKD III
Baseline Cr 0.7, p/w 1.3 >> 1.5
Volume status: Euvolemic
Electrolytes: Stable
Blood pressure: WNL but soft
Hb: stable at 9.2, anemic
- LR 75 cc/h x 12hours
- 25% albumin q8h for 1 day
- Urine electrolytes
- Urine microscopic analysis