AM Report 1/31/17: PD Peritonitis and Shock Liver

Steps to an Acid/Base Problem:

  1. Step 1: Check for internal consistency[H+] = 24 x pC02/HCO3
  2. Step 2: Use pH to determine primary disorder
  3. Step 3: Calculate the AGAG = [Na+] – [Cl- + HCO3]
  4. Step 4: Determine the presence of additional disordersCorrected HCO3 = measured HCO3 + [AG – 12]
  5. Step 5: Calculate the expected pC02 for metabolic acidosis (Winter’s Formula)Expected PC02 = 1.5 (HCO3) +8 +/- 2

5 Etiologies with AST/ALT elevations > 1000:

  • Drugs/Toxins (acetaminophen, toxic mushrooms, etc.)
  • Hepatic ischemia
  • Acute viral hepatitis
  • Acute autoimmune hepatitis
  • Wilson disease

3 components that define acute liver injury:

  • Elevated aminotransferases
  • Hepatic encephalopathy
  • Elevated PT/INR

*No preexisting cirrhosis or liver disease; <26 weeks

Acetaminophen Toxicity:

  • 4 grams is the daily maximum recommended dose
  • N-acetylcysteine is the treatment of choice in suspected acetaminophen toxicity -nmay be given IV, using a 20 hour protocol, or orally, using a 72 hour protocol
  • Use the Rumack-Matthew nomogram to elevate for poisoning severity

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Options for renal replacement therapy (RRT):

  • Hemodialysis
  • Peritoneal dialysis
  • Transplantation
  • Non-dialytic management – manage symptoms and focus on QOL

Peritoneal dialysis – a dialysate solution is intermittently instilled into the peritoneal cavity via an indwelling catheter, and excess water/solutes are removed by osmosis and diffusion across the peritoneal membrane into the dialysis solution.

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Two different options for PD exist:

  1. Continuous ambulatory peritoneal dialysis (CAPD)
  2. Automated peritoneal dialysis (APD)

    *CAPD does not require a machine, while APD relies on a “cycler” to fill and empty your belly 3-5 times during the night

    *There is no difference in clinical outcome between PD and HD – although there is a trend toward superior outcomes for PD patients with new-onset ESRD who have residual kidney function

Potential complications with PD:

  • Peritonitis – from frequent access via the catheter or from perforation or microperforation of bowel
  • Hernias at catheter site
  • Subcutaneous edema
  • Difficulty draining catheter (often due to constipation)
  • Pleural effusions
  • Sclerosing peritonitis: scarring/fibrosis from recurrent peritonitis – can lead to bowel constriction.  Prognosis is extremely poor (often fatal) and treatment requires surgical stripping.

Diagnosis of peritonitis requires 2 out of 3 of the following:

  • Clinical signs of peritonitis
  • Peritoneal fluid WBC > 100 cells/mm3 with >50% PMNs
  • Positive peritoneal fluid culture

Common clinical manifestations of PD related peritonitis:

  • Abdominal pain (79-88%)
  • Cloudy peritoneal effluent (84%)
  • Fever (>37.5 C) (29-53%)
  • Nausea/Vomiting (31-51%)
  • Hypotension (~18%)

Most common organisms of peritonitis in PD patients:

  • Gram-positive organisms ~ 50% -Coagulase-negative staph (S. epidermidis) and S. aureus
  • Gram-negative organisms ~ 15%
  • Fungal ~2%
  • Polymicrobial ~ 4%
  • Culture negative ~ 20%

Empiric Antibiotic Regimen:

  • Gram positive coverage – typically Vancomycin (or 1st generation cephalosporin)
  • Gram negative coverage – typically 3rd generation cephalosporin
  • Fungal prophylaxis while on ABX – typically nystatin

Indications for PD catheter removal:

  • Relapsing peritonitis – episode of peritonitis with the same organism that caused the preceding episode within 4 weeks of completing antibiotics
  • Refractory peritonitis – peritonitis that does not respond to appropriate antibiotics within 5 days
  • Refractory catheter infection – exit-site/tunnel infections
  • Fungal or mycobacterial peritonitis

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