Hyponatremia

HPI:

A 62 year-old male with a history of hepatitis C cirrhosis complicated by hepatocellular carcinoma s/p radiofrequency ablation presenting after referral from hepatology clinic for hyponatremia. One week ago, the patient developed abdominal distension and shortness of breath that resolved after large-volume paracentesis and was started on furosemide 40mg p.o. daily and aldactone 100mg p.o. daily. After initiating diuretics, the patient noted worsening lower extremity edema, and increased thirst/fluid intake.

He reports two days of fatigue and intermittent confusion supported by family members who reported slowed speech. He otherwise denies abdominal pain, distension, nausea/vomiting, diarrhea/constipation, chest pain or shortness of breath. In the ED, the patient received 1L NS bolus.

PMH:

Hepatitis C cirrhosis c/b HCC s/p RFA
Rheumatoid arthritis

PSH:

None

Family History:

Non-contributory.

Social History:

Lives with partner, denies current or prior t/e/d abuse
HepC contracted from blood transfusions

Medications:

Furosemide 40mg p.o. daily
Spironolactone 100mg p.o. daily
Rifaximin 550mg p.o. b.i.d.

Allergies:

NKDA

Physical Exam:

VS:	T	98.2	HR	80	RR	14	BP	95/70	O2	98% RA
Gen:	Elderly male in no acute distress, alert and answering questions appropriately.
HEENT:	NC/AT, PERRL, EOMI, faint scleral icterus, MMM.
CV:	RRR, normal S1/S2, no murmurs. JVP 8cm.
Lungs:	Faint basilar crackles on bilateral lung bases.
Abd:	Normoactive bowel sounds, mildly distended but non-tender, without rebound/guarding.
Ext:	2+ pitting edema in lower extremities to knees bilaterally. 2+ peripheral pulses, warm and well perfused.
Neuro:	AAOx3. CN II-XII intact. No asterixis. Normal gait. Normal FTN/RAM.

Labs/Studies:

BMP (admission): 112/5.6/88/22/28/1.1/97
BMP (+10h): 118/5.4/93/23/26/1.0/133
sOsm: 264
Urine: Na <20, K 26, Osm 453
BNP: 40
AST/ALT/AP/TB/Alb: 74/57/91/2.4/2.2

Assessment/Plan:

62M with HepC cirrhosis, with e/o decompensation (new-onset ascites) and hyponatremia.

#Hyponatremia: Sodium 114, likely chronic, patient currently asymptomatic without concerning findings on neurological exam. Clinical findings suggestive of hypervolemic hyponatremia 2/2 decompensated cirrhosis resulting in decreased effective arterial blood volume and volume retention. However, the recent initiation of diuretics, mild AKI and early response to isotonic fluids in the ED suggests possible hypovolemic component.
- 1L fluid restriction
- q.4.h. sodium check, goal increase of 8mEq per 24h
- hold diuretics
#Hyperkalemia: Potassium 5.6, asymptomatic, AKI vs. medication-induced (aldactone). Continue monitoring.
#AKI: Elevated creatinine 1.1 from baseline 0.7. Likely pre-renal given recent initiation of diuretics. Consider hepatorenal syndrome given decompensated cirrhosis. Follow-up repeat creatinine after 1L NS bolus in ED.
#Hepatitis C: decompensated with new-onset ascites. No e/o encephalopathy, continue home rifaximin.

Physiology of Hyponatremia: ^1,2,3,4

Differential Diagnosis of Hyponatremia: ⁵

Evaluation of Hyponatremia: ²

Identification of onset (acute vs. chronic)
Presence of symptoms (HA, nausea, confusion, seizures)
Assessment of volume status (edema, JVD, skin turgor, postural BP)
Medical history (cardiac, liver, renal disease), drug history

References:

Freda BJ, Davidson MB, Hall PM. Evaluation of hyponatremia: a little physiology goes a long way. Cleve Clin J Med. 2004;71(8):639–650.
Biswas M, Davies JS. Hyponatraemia in clinical practice. Postgrad Med J. 2007;83(980):373–378. doi:10.1136/pgmj.2006.056515.
Adrogué HJ, Madias NE. Hyponatremia. N. Engl. J. Med. 2000;342(21):1581–1589. doi:10.1056/NEJM200005253422107.
Marx JA, Hockberger RS, Walls RM, Adams JG. Rosen’s emergency medicine: concepts and clinical practice. 2010;1.
Milionis HJ, Liamis GL, Elisaf MS. The hyponatremic patient: a systematic approach to laboratory diagnosis. CMAJ. 2002;166(8):1056–1062.

Thrombocytopenia

Brief HPI:

A middle-aged female with no known medical history is brought to the emergency department with altered mental status. Her family notes worsening confusion over the past 2-3 days associated with vomiting and yellow discoloration of skin and eyes.

Initial vital signs were normal, though with borderline hypotension (99/64mmHg). Examination demonstrated an alert, but lethargic patient with jaundice and scleral icterus, no skin lesions were appreciated. Laboratory studies were obtained:

CBC

WBC: 21.3 (N: 83%, Bands: 11%)
Hb: 5.5
Plt: 6k
Marked schistocytes

Coagulation Panel

INR: 1.26
PTT: Normal
Fibrinogen: Normal
FDP: Normal
D-dimer: >9,000 (normal 250)
Haptoglobin: Undetectable
LDH: 1493

CMP

Creatinine: 1.1
AST/ALT: Normal
TB: 4.3, DB: 0.8

Imaging:

CT Head: No acute intracranial process.

CT Abdomen/Pelvis with Contrast

Moderate free intra-abdominal fluid, heterogeneous liver with periportal edema, dense right middle lobe consolidation.

ED Course:

The patient developed worsening respiratory failure with hypoxia and tachypnea requiring endotracheal intubation. Thrombotic thrombocytopenic purpura was suspected and while awaiting emergent plasma exchange transfusion, the patient arrested and resuscitation efforts were unsuccessful.

The patient’s ADAMTS13 activity level was <3%. Autopsy demonstrated consolidation of the right middle lobe with possible lymphoproliferative mass, and lung petechial hemorrhages from microvascular thrombi.

Differential Diagnosis of Thrombocytopenia ^1-7

Algorithm for the Evaluation of Thrombocytopenia ⁸

Definition ⁹

Mild: <150k
Moderate: 100-150k
Severe: <50k
- 10-30k: bleeding with minimal trauma
- <10k: increased risk spontaneous bleeding

History ^9,10

Prior platelet count
Family history bleeding disorders
Medications
- Heparin
- Quinine, quinidine
- Rifampin
- Trimethoprim-sulfamethoxazole
- Vancomycin
Alcohol use
Travel-related infections

Physical Examination ^9,10

Splenomegaly (liver disease)
Lymphadenopathy (infection, malignancy)

Workup ^10,11

Red blood cell fragments (schistocytes) ¹¹

hCG
Repeat CBC
- Detect spurious measure
- Neutrophil-predominant leukocytosis: bacterial infection
- Immature leukocytes (blasts): leukemia, myelodysplasia
Peripheral smear
- Schistocytes: microangiopathic process (DIC, TTP, HUS)
- Atypical lymphocytes: viral infection
- Intracellular parasites: malaria
- Hypersegmented neutrophils: nutritional deficiency
Infectious features: HIV, HCV, EBV, H.pylori, blood cultures
Autoimmune features: ANA, APL-Ab
Suspected occult liver disease: LFT, PT/PTT/INR
Suspected thrombotic microangiopathy: PT/PTT/INR, haptoglobin, LDH, fibrinogen, FDP, d-dimer

Specific Conditions ^2-6,9,12-20

Disease	Cause	Presentation	Laboratory Findings	Treatment
DIC	Sepsis Trauma Burn Malignancy	Bleeding Multi-organ failure Shock	INR Fibrinogen FDP D-dimer	Directed at underlying cause Transfusion thresholds for hemorrhage: FFP for INR >1.5 Platelets if <50k Cryoprecipitate of fibrinogen <100mg/dL
TTP	Insufficient ADAMTS-13 activity	Non-specific constitutional symptoms (ex. weakness) Neuro: headache, AMS, focal neuro deficit GI: abdominal pain, nausea/vomiting	LDH Reticulocyte Unconjugated bilirubin Haptoglobin	Plasma exchange
HUS	Shiga-toxin-producing bacteria, E. coli O157:H7	Bloody diarrhea, anuria, oliguria, and hypertension	LDH Reticulocyte Unconjugated bilirubin Haptoglobin	Aggressive supportive care
HELLP	Spectrum of eclampsia	Hypertension Visual symptoms Headache RUQ abdominal pain	AST/ALT Uric acid Unconjugated bilirubin LDH Reticulocyte Haptoglobin	Delivery, MgSO4
ITP	Primary ITP Secondary ITP – Drug – Autoimmune – Infection – Malignancy	Usually asymptomatic, may have petechiae or easy bruising	Isolated thrombocytopenia	Steroids
HIT	Exposure to heparin or LMWH	Thrombocytopenia or a 50 percent reduction in platelet count between 5-10d exposure New thrombosis or skin necrosis 4 T’s score	Platelet factor 4 antibodies	Withdraw heparin

References

Greinacher A, Selleng S. How I evaluate and treat thrombocytopenia in the intensive care unit patient. Blood. 2016;128(26):3032-3042. doi:10.1182/blood-2016-09-693655.
Joly BS, Coppo P, Veyradier A. Thrombotic thrombocytopenic purpura. Blood. 2017;129(21):2836-2846. doi:10.1182/blood-2016-10-709857.
Leslie SD, Toy PT. Laboratory hemostatic abnormalities in massively transfused patients given red blood cells and crystalloid. Am J Clin Pathol. 1991;96(6):770-773.
Neunert C, Lim W, Crowther M, et al. The American Society of Hematology 2011 evidence-based practice guideline for immune thrombocytopenia. Blood. 2011;117(16):4190-4207. doi:10.1182/blood-2010-08-302984.
Kappler S, Ronan-Bentle S, Graham A. Thrombotic microangiopathies (TTP, HUS, HELLP). Emerg Med Clin North Am. 2014;32(3):649-671. doi:10.1016/j.emc.2014.04.008.
Greinacher A. Heparin-Induced Thrombocytopenia. Solomon CG, ed. N Engl J Med. 2015;373(3):252-261. doi:10.1056/NEJMcp1411910.
Reardon JE Jr., Marques MB. Evaluation of Thrombocytopenia. Lab Med. 2006;37(4):248-250. doi:10.1309/R7P79KERAJHPRHLT.
Stasi R. How to approach thrombocytopenia. Hematology Am Soc Hematol Educ Program. 2012;2012:191-197. doi:10.1182/asheducation-2012.1.191.
Gauer RL, Braun MM. Thrombocytopenia. Am Fam Physician. 2012;85(6):612-622.
Abrams CS. 172 – Thrombocytopenia. Twenty Fifth Edition. Elsevier Inc.; 2016:1159–1167.e2. doi:10.1016/B978-1-4557-5017-7.00172-0.
Wilson CS, Vergara-Lluri ME, Brynes RK. Chapter 11 – Evaluation of Anemia, Leukopenia, and Thrombocytopenia. Second Edition. Elsevier Inc.; 2017:195-234.e195. doi:10.1016/B978-0-323-29613-7.00011-9.
Hui P, Cook DJ, Lim W, Fraser GA, Arnold DM. The frequency and clinical significance of thrombocytopenia complicating critical illness: a systematic review. Chest. 2011;139(2):271-278. doi:10.1378/chest.10-2243.
Jokiranta TS. HUS and atypical HUS. Blood. 2017;129(21):2847-2856. doi:10.1182/blood-2016-11-709865.
Neunert CE. Management of newly diagnosed immune thrombocytopenia: can we change outcomes? Hematology Am Soc Hematol Educ Program. 2017;2017(1):400-405. doi:10.1182/asheducation-2017.1.400.
Lambert MP, Gernsheimer TB. Clinical updates in adult immune thrombocytopenia. Blood. 2017;129(21):2829-2835. doi:10.1182/blood-2017-03-754119.
Arepally GM. Heparin-induced thrombocytopenia. Blood. 2017;129(21):2864-2872. doi:10.1182/blood-2016-11-709873.
Aster RH, Bougie DW. Drug-induced immune thrombocytopenia. N Engl J Med. 2007;357(6):580-587. doi:10.1056/NEJMra066469.
Boral BM, Williams DJ, Boral LI. Disseminated Intravascular Coagulation. Am J Clin Pathol. 2016;146(6):670-680. doi:10.1093/ajcp/aqw195.
Scully M, Hunt BJ, Benjamin S, et al. Guidelines on the diagnosis and management of thrombotic thrombocytopenic purpura and other thrombotic microangiopathies. Br J Haematol. 2012;158(3):323-335. doi:10.1111/j.1365-2141.2012.09167.x.
Levine RL, Hursting MJ, Drexler A, Lewis BE, Francis JL. Heparin-induced thrombocytopenia in the emergency department. Ann Emerg Med. 2004;44(5):511-515. doi:10.1016/j.annemergmed.2004.06.004.

Acute Urinary Retention

Brief H&P:

A 62 year-old male with no significant medical history, presented to the emergency department with several days of vomiting. Examination showed suprapubic fullness with tenderness to palpation and a bedside ultrasound was performed:

RUQ

Right upper quadrant ultrasound with moderate hydronephrosis.

LUQ

Left upper quadrant ultrasound with moderate hydronephrosis.

Bladder

Relatively non-distended bladder.

Bladder Volume

Post-void bladder volume.

Ultrasound revealed moderate bilateral hydronephrosis with a relatively non-distended bladder. Labs were notable for new renal failure and the patient was admitted for continued evaluation. He was ultimately diagnosed with idiopathic retroperitoneal fibrosis with bilateral distal ureteral obstruction requiring stenting.

Anatomy of Acute Urinary Retention:

Differential Diagnosis of Acute Urinary Retention:^1,2,3

Acute Kidney Injury

Hospital Course:

64 year-old female with a history of metastatic colonic adenocarcinoma was initially admitted for PO intolerance secondary to recurrent small bowel obstructions (associated with abdominal tumor burden). On hospital day six, the patient developed tachypnea, hypoxemia, hypotension and was intubated for respiratory distress. In the MICU, the patient was treated for acute hypoxic respiratory failure thought to be caused by aspiration (large volume bilious emesis prior to intubation despite NGT LCWS) vs. accumulating malignant pleural effusions vs. pulmonary embolism. Septic shock of a presumed pulmonary vs. intra-abdominal source was managed with vasopressors and broad-spectrum antimicrobials.

On hospital day fourteen, an elevation in the serum creatinine was noted. Known nephrotoxic agents include iodinated contrast on hospital day five, and vancomycin. The patient’s vasopressor requirement had decreased to norepinephrine 6mcg/kg/min (previously requiring four vasopressors). Over the next six days, the serum creatinine continued to trend upwards associated with a decrease in urine output (0.3-0.5mL/kg/hour). Intravenous crystalloid and colloid administered liberally based on central venous pressure and ultrasound of the inferior vena cava did not impact urine output.

Laboratory Studies

Hospital day	19	18	17	16	15	14	3
Creatinine	1.72	1.59	1.46	1.32	1.24	1.09	0.75
Vancomycin	23.5	28.5	36.3	45.5	47.7		22.1

Urine electrolytes:

Una: 10
Ucr: 180
Uk: 13
Ucl: 22
Uur: 265
FeNa: <1%

UA: 3+LE, 1+ blood, 36WBC, 14RBC, 3+ bacteria, amorphous crystals

Imaging:

CT Abdomen/Pelvis with IV contrast

Within the retroperitoneum, the left kidney is small and atrophic and demonstrates limited peripheral enhancement. The left renal artery is also poorly visualized.
Severely dilated loops of small bowel, including a segment within the left lower quadrant that may represent a closed loop obstruction.
There is a large (16.4 cm in largest diameter) subphrenic fluid collection in the left upper quadrant. A second large (14.2 cm in largest diameter) intraabdominal fluid collection lies inferior and anteriorly.

Assessment:

Oliguric acute renal failure in the setting of convincingly pre-renal urine studies which was not responsive to adequate crystalloid and colloid volume resuscitation. The patient had a normal ejection fraction on a recent echocardiogram, and while the patient was hypoalbuminemic (presumably from poor nutritional status and PO intolerance), urine output was not even transiently responsive to colloid administration. While the patient had recent administration of intravenous contrast, the elevation in serum creatinine occurred more than one week later. Further, the elevated vancomycin trough was likely a consequence rather than the etiology of worsening renal failure. AKI was likely secondary to renal artery compression from mass effect associated with abdominal metastases. There was evidence of a similar process affecting the left kidney, which was severely atrophic. The patient declined further evaluation, which would have included a renal ultrasound.

Definition of Acute Kidney Injury: ¹

Elevation of serum creatinine > 0.3mg/dL in 48h
Elevation of serum creatinine > 1.5x baseline in 7d
Oliguria (UOP < 0.5mL/kg/hr) > 6h

Staging of Acute Kidney Injury: ¹

Stage	Creatinine	UOP
1	1.5-1.9x	<0.5mL/kg/hr for 6-12h
2	2.0-2.9x	<0.5mL/kg/hr for >12h
3	3.0x or RRT	<0.3mL/kg/hr for > 24h

Management of Contrast-induced AKI: ²

Administer lowest dose
Use iso-osmolar, or low-osmolar contrast
Volume expansion (NaCl, NaHCO3)
PO NAC questionable benefit but likely harmless

Differential Diagnosis of Acute Kidney Injury: ³

NOTE: Algorithm revised in November, 2017. The prior version is no longer supported but remains available here.

Evaluation of AKI: ⁴

Condition	Urinalysis	Casts	FeNa (%)
Pre-renal	Normal	Hyaline	<1
Intra-renal
ATN	Mild proteinuria	Pigmented granular	>1
AIN	Mild proteinuria, Hb, WBC	WBC casts, eosinophils	>1
GN	Moderate/severe proteinuria, Hb	RBC casts	<1
Post-renal	Normal	Crystals	>1

References:

Kellum, J. A., Lameire, N., KDIGO AKI Guideline Work Group. (2013). Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Critical care (London, England), 17(1), 204. doi:10.1186/cc11454
Lameire, N., Kellum, J. A., KDIGO AKI Guideline Work Group. (2013). Contrast-induced acute kidney injury and renal support for acute kidney injury: a KDIGO summary (Part 2). Critical care (London, England), 17(1), 205. doi:10.1186/cc11455
Lameire, N., Van Biesen, W., & Vanholder, R. (2005). Acute renal failure. Lancet, 365(9457), 417–430. doi:10.1016/S0140-6736(05)17831-3
Thadhani, R., Pascual, M., & Bonventre, J. V. (1996). Acute renal failure. New England Journal of Medicine, 334(22), 1448–1460. doi:10.1056/NEJM199605303342207
WikEM: Acute kidney injury

Renal Failure in Cirrhosis

CC:

Consult for acute kidney injury

HPI:

63M with a history of liver cirrhosis of cryptogenic etiology, portal vein thrombosis, and esophageal varices s/p banding (2011) who was admitted to an OSH for altered mental status and hypotension requiring dopamine and was transferred to this facility for a higher level of care.

The nephrology service was consulted for elevated serum creatinine concerning for AKI. The patient has a baseline creatinine of 1.1 (3/2013), 1.9 on transfer and continued worsening to peak of 2.6 today.

PMH:

Asthma
COPD
Cirrhosis (PVT, encephalopathy)
Inguinal hernia (recurrent)

PSH:

Appendectomy
Bilateral inguinal hernia repair

FH:

Non-contributory

SHx:

Married
Denies t/e/d use

Meds:

albumin 25g i.v. q.6.h.
erythromycin 1,000mg p.o. q.1.h.
fluticasone-salmeterol 1 puff b.i.d.
lactulose 45g p.o. q.6.h.
neomycin 1,000mg p.o. q.1.h.
pantoprazole 40mg i.v. daily
rifaximin 550mg p.o. b.i.d.
sodium benzoate 5g p.o. b.i.d.

Allergies:

Sulfa

Physical Exam:

VS:	T	37.4	HR	90	RR	15	BP	86/48	O2	97% RA
Gen:	Chronically ill-appearing.
HEENT:	PERRL, scleral icterus, MMM
CV:	RRR
Lungs:	CTAB
Abd:	+BS, soft, non-tender, non-distended
GU:	Large ascites filled scrotum, testicles/inguinal canal not easily palpated
Ext:	Warm, well-perfused
Skin:	No palmar erythema, no vascular spiders
Neuro:	AAOx4, CN II-XII grossly intact

Labs:

BMP: 134/4.5/103/20/41/3.0/106 (Ca 9.3, Mg 3.7, PO4 2.4)
LFT: AST 89, ALT 33, TB 26.6, CB 16.1, Alb 2.7
NH4 167

Imaging:

Pleural Effusion

Large right pleural effusion with underlying compressive atelectasis.

Cirrhosis and Portal Hypertension

Shrunken/nodular liver with sequelae of portal hypertension including perisplenic collaterals, and splenomegaly.

SMV Thrombosis

Near-total thrombosis of the portal vein extending down to superior mesenteric vein.

B/L Inguinal Hernias

Large volume abdominal ascites with a large amount of fluid extending into the bilateral inguinal canals.

Large Right Inguinal Hernia

Large volume abdominal ascites with a large amount of fluid extending into the bilateral inguinal canals.

CT Abdomen/Pelvis (PVT)

Assessment/Plan:

63M with a history of liver cirrhosis of cryptogenic etiology, recently with hypotension prior to transfer to this facility and increase in creatinine from 1.9-3.0 on current admission (from baseline 1.1).

These findings indicate acute kidney injury, likely hepatorenal syndrome vs. acute tubular necrosis 2/2 prolonged hypotension. Plan to discontinue diuretics and start albumin challenge (1g/kg/day divided q6h x2d). Will also check UA, urine Na/cr/urea/eos, renal US (evaluate obstruction, kidney size). Start midodrine/octreotide for underlying HRS.

Neuro: Intermittent confusion. Lactulose, rifaximin, benzoate.
Resp: 2L NC. ABG 7.36/51/87/27.7/+2. CXR: Large R effusion.
CV: Levo 0.075. Midodrine 15 TID. MAPs 60, HR 80s.
GI: NPO/NGT. TPN.
Renal: See above.
Heme: Coagulopathy, keep INR <2.5
ID: Afebrile. No abx.
Endo: Euglycemic

Renal Failure in Cirrhosis:

Renal failure in cirrhosis is associated with higher mortality both before and after transplant. The main causes of renal failure in cirrhosis are detailed below, with particular attention to an entity unique to cirrhosis: the hepatorenal syndrome.¹

Disorder	Pathogenesis	Diagnosis	Management
HRS	Dilation of splanchnic arteries initially compensated by increased CO eventually decompensates with activation of mechanisms to preserve ECBV (RAAS, SNS, ADH) leading to fluid retention (ascites, edema) and renal failure due to intrarenal vasoconstriction.Bacterial translocation and the resulting inflammatory response may contribute to splanchnic vasodilation (through production of vasoactive factors like NO).	Serum creatinine > 1.5mg/dl- Not reduced with 1g/kg albumin No confounding factors (2d off diuretics, no nephrotoxic agents, no shock, no e/o intrinsic renal disease) Type 1: doubling creatinine > 2.5mg/dL in <2wk Type 2: stable, slower progression	Vasoconstrictor therapy- Albumin Portasystemic shunting Renal replacement therapy Prevention Norfloxacin Albumin
Intrinsic renal	Some causes of liver disease are also associated with intrinsic renal pathology (ex. GN associated with HBV, HCV).	Proteinuria, hematuria Renal bx Active urinary sediment	Antiviral therapy if appropriate
Pre-renal AKI	Hemorrhage (GIB), fluid losses (excess diuresis, diarrhea from lactulose).	Suspected from patient history Low FENa, bland urine sediment	Hemorrhage: replace volume with fluids, blood products. Control bleeding. Discontinue diuretics, administer fluids if tolerated
ATN	Severe ischemic or toxic (NSAID’s, nephrotoxic medications)	Renal tubular epithelial cells favor ATN (granular casts common in ATN, HRS)	Withdraw therapy Avoid nephrotoxic agents

Pathophysiology of Hepatorenal Syndrome:

Evaluation:

The evaluation of suspected renal failure in patients with cirrhosis involves assessment of renal function for evidence of acute impairment, as well as analaysis of urine for protein or active sediment to suggest intrinsic renal disease (possibly warranting renal ultrasonography or biopsy). Additionally, patients should be evaluated for evidence of bacterial infection including assessment of ascites if present as SBP produces a more severe form of the inflammatory vasodilation mechanism suspected to play a role in HRS.

Treatment:

For renal failure not caused by the hepatorenal syndrome, identification and management of the underlying cause is critical (intrinsic renal disease, hypovolemia/hemorrhage, nephrotoxicity, infection). For suspected HRS, management is dependent on the acuity and setting. In the intensive care unit, vasoconstrictor therapy (norepinephrine, vasopressin) in association with albumin is effective in the treatment of HRS.^2,3 In less acute settings, a combination of midodrine, octreotide and albumin improves renal function and is associated with lower short-term mortality.⁴ Alternatives for patients who do not respond to medical therapy include TIPS, dialysis and transplant.

Summary:

Renal failure in ESLD is due to the causes, complications or management of cirrhosis and has important implications, with HRS in particular offering the worst prognosis.⁵ Early recognition and management is critical to improving outcomes.

References:

Ginès, P., & Schrier, R. W. (2009). Renal failure in cirrhosis. The New England journal of medicine, 361(13), 1279–1290. doi:10.1056/NEJMra0809139
Singh, V., Ghosh, S., Singh, B., Kumar, P., Sharma, N., Bhalla, A., Sharma, A. K., et al. (2012). Noradrenaline vs. terlipressin in the treatment of hepatorenal syndrome: a randomized study. Journal of hepatology, 56(6), 1293–1298. doi:10.1016/j.jhep.2012.01.012
Kiser, T. H., Fish, D. N., Obritsch, M. D., Jung, R., MacLaren, R., & Parikh, C. R. (2005). Vasopressin, not octreotide, may be beneficial in the treatment of hepatorenal syndrome: a retrospective study. Nephrology, dialysis, transplantation, 20(9), 1813–1820. doi:10.1093/ndt/gfh930
Esrailian, E., Pantangco, E. R., Kyulo, N. L., Hu, K.-Q., & Runyon, B. A. (2007). Octreotide/Midodrine therapy significantly improves renal function and 30-day survival in patients with type 1 hepatorenal syndrome. Digestive diseases and sciences, 52(3), 742–748. doi:10.1007/s10620-006-9312-0
Alessandria, C., Ozdogan, O., Guevara, M., Restuccia, T., Jiménez, W., Arroyo, V., Rodés, J., et al. (2005). MELD score and clinical type predict prognosis in hepatorenal syndrome: relevance to liver transplantation. Hepatology (Baltimore, Md.), 41(6), 1282–1289. doi:10.1002/hep.20687

HPI:

PMH:

PSH:

Family History:

Social History:

Medications:

Allergies:

Physical Exam:

Labs/Studies:

Assessment/Plan:

Physiology of Hyponatremia: 1,2,3,4

Differential Diagnosis of Hyponatremia: 5

Evaluation of Hyponatremia: 2

References:

Brief HPI:

CBC

Coagulation Panel

CMP

Imaging:

CT Abdomen/Pelvis with Contrast

ED Course:

Differential Diagnosis of Thrombocytopenia 1-7

Algorithm for the Evaluation of Thrombocytopenia 8

Definition 9

History 9,10

Physical Examination 9,10

Workup 10,11

Specific Conditions 2-6,9,12-20

References

Brief H&P:

RUQ

LUQ

Bladder

Bladder Volume

Anatomy of Acute Urinary Retention:

Differential Diagnosis of Acute Urinary Retention:1,2,3

Hospital Course:

Laboratory Studies

Imaging:

CT Abdomen/Pelvis with IV contrast

Assessment:

Definition of Acute Kidney Injury: 1

Staging of Acute Kidney Injury: 1

Management of Contrast-induced AKI: 2

Differential Diagnosis of Acute Kidney Injury: 3

Evaluation of AKI: 4

References:

CC:

HPI:

PMH:

PSH:

FH:

SHx:

Meds:

Allergies:

Physical Exam:

Labs:

Imaging:

Pleural Effusion

Cirrhosis and Portal Hypertension

SMV Thrombosis

B/L Inguinal Hernias

Large Right Inguinal Hernia

CT Abdomen/Pelvis (PVT)

Assessment/Plan:

Renal Failure in Cirrhosis:

Pathophysiology of Hepatorenal Syndrome:

Evaluation:

Treatment:

Summary:

References:

Physiology of Hyponatremia: ^1,2,3,4

Differential Diagnosis of Hyponatremia: ⁵

Evaluation of Hyponatremia: ²

Differential Diagnosis of Thrombocytopenia ^1-7

Algorithm for the Evaluation of Thrombocytopenia ⁸

Definition ⁹

History ^9,10

Physical Examination ^9,10

Workup ^10,11

Specific Conditions ^2-6,9,12-20

Differential Diagnosis of Acute Urinary Retention:^1,2,3

Definition of Acute Kidney Injury: ¹

Staging of Acute Kidney Injury: ¹

Management of Contrast-induced AKI: ²

Differential Diagnosis of Acute Kidney Injury: ³

Evaluation of AKI: ⁴