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

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.

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