CCRN GI, Renal and Skin Review: GI Bleeding, Abdominal Compartment Syndrome, AKI Staging and Nephrotoxic Drugs

Abdominal and kidney problems in the ICU often announce themselves through other systems: a blood pressure that won't hold, airway pressures that creep up, a urine bag that stays nearly empty. That is why CCRN items in this area hand you vital signs and numbers and ask what they mean. This review follows the GI, renal and integumentary lists in Category C, using the guidelines and MSD Manual chapters named in each section, opened on October 28, 2026. It gives no drug doses.

What Category C lists under GI, renal and integumentary

The Adult CCRN test plan (exams on and after November 12, 2025) lists:

• Gastrointestinal: abdominal compartment syndrome, acute abdominal trauma, acute GI hemorrhage, bowel infarction, obstruction or perforation (mesenteric ischemia and adhesions are the examples), GI surgeries, hepatic failure and coma, liver disease, malnutrition and malabsorption, pancreatitis, peritonitis.
• Renal and genitourinary: acute kidney injury and acute tubular necrosis, chronic kidney disease, infections such as urosepsis.
• Integumentary: cellulitis, IV infiltration, necrotizing fasciitis, pressure injury, skin failure, wounds.

The matching testable nursing actions include EGD, enteral and parenteral nutrition, enteral tubes and GI drains; identifying nephrotoxic agents and managing hemodialysis, CRRT and peritoneal dialysis; pressure-injury prevention and devices such as wound VACs, pressure-reduction surfaces, ostomy and fecal management devices and IV infiltrate treatment. Intra-abdominal pressure monitoring appears under Multisystem actions. Together with endocrine and hematology, this is the largest category on the exam.

Acute GI hemorrhage: stabilize first, then find the source

The MSD Manual's GI bleeding overview (full review June 2025) treats hematemesis, hematochezia or melena as a potential emergency, managed in an ICU or other monitored setting with a gastroenterologist and a surgeon involved for severe bleeding. Its treatment points, in the order the chapter presents them:

1. Airway. Aspiration of blood is a major cause of morbidity and death in active upper GI bleeding, so MSD says intubation should be considered in patients with an inadequate gag reflex or who are obtunded, particularly before endoscopy.
2. Access and volume. Short, large-bore peripheral catheters (14- to 16-gauge) are preferable to a central line unless a large sheath is used, and IV fluids start immediately, followed by packed red cells if more resuscitation is needed.
3. Transfusion targets. MSD says transfusion in older adults or patients with coronary disease may stop when hemoglobin is stable at 8 g/dL unless they're symptomatic, while younger patients or those with chronic bleeding usually aren't transfused unless hemoglobin is below 7 g/dL or they have symptoms such as dyspnea or coronary ischemia. A large transfusion follows the institution's massive transfusion protocol with plasma and platelets.
4. Medications by suspected source. An IV proton pump inhibitor may be started for possible upper GI bleeding and should be used if an ulcer is confirmed; octreotide is used for suspected variceal bleeding.

Bedside facts that change answers:

• Melena takes volume. About 100 to 200 mL of blood in the upper GI tract causes melena, which can persist for days after bleeding stops. Iron and bismuth also blacken stool without blood.
• A clean aspirate doesn't rule it out. MSD says nasogastric aspiration is done in suspected upper GI bleeding, but up to 15% of patients with upper GI bleeding have no blood in the aspirate; coffee-ground material means slow or stopped bleeding.
• Skip orthostatic checks in severe bleeding. MSD calls them unwise in that setting because they can cause syncope, and unreliable as a volume measure.
• Liver disease raises the stakes. GI bleeding in a patient with liver disease may precipitate portosystemic encephalopathy or hepatorenal syndrome.

A fictional Passy vignette. A man with cirrhosis vomits bright red blood twice. His heart rate is 124/min, blood pressure 88/52 mm Hg, and he is drowsy. Following MSD's order, the first nursing moves are airway protection with a call for help (a drowsy patient vomiting blood is the aspiration risk MSD describes), short large-bore IV access with fluids and then blood as ordered, and preparation for octreotide, a PPI and rapid endoscopy as the team orders. His drowsiness also deserves a plan: blood in the gut is one of the triggers MSD lists for encephalopathy. When a vignette like this trips you, a planned explanation for every option, right or wrong, shows which priority you skipped.

Acute pancreatitis: moderate fluids, early feeding, no routine antibiotics

MSD's acute pancreatitis chapter (full review August 2026) classifies severity by organ failure: moderately severe disease has local or systemic complications without organ failure or with transient failure that resolves within 48 hours, and severe disease has persistent organ failure beyond 48 hours. Systemic inflammation can cause ARDS and acute kidney injury. The current treatment points:

• Fluids. Resuscitation with a moderate volume of lactated Ringer's solution, reassessed frequently in the first 6 hours and over the next 24 to 48 hours. MSD judges adequacy by falling hematocrit and BUN, better vital signs and urine output, and notes that a BUN that stays high despite resuscitation signals higher morbidity and mortality.
• Pain. Parenteral opioids in adequate doses, with antiemetics.
• Nutrition. Early enteral nutrition, because it is associated with lower morbidity than delayed or no feeding; enteral feeding is preferred over parenteral.
• Antibiotics. Per guidelines MSD cites, prophylactic antibiotics aren't recommended at any severity; they're started for an extrapancreatic infection or infected necrosis.

MSD also lists hyperglycemia and hypocalcemia among the lab findings, and says hypomagnesemia should be excluded in a hypocalcemic patient. Grey Turner and Cullen signs are rare (under 3%) and carry a poor prognosis.

Mesenteric ischemia: pain out of proportion to the exam

MSD's chapter on acute mesenteric ischemia (full review July 2024) gives the classic early picture: severe abdominal pain with minimal physical findings, a soft abdomen with little tenderness, perhaps mild tachycardia. Peritoneal signs, absent bowel sounds and shock come later, as the bowel infarcts, and mortality rises sharply once infarction has occurred. Risk factors include coronary disease, heart failure, valve disease, atrial fibrillation and previous arterial emboli, and MSD says the diagnosis must be considered in anyone over 50 with risk factors who develops sudden, severe abdominal pain. Lactate and creatine kinase rise with necrosis but are late, nonspecific findings, so a normal lactate early doesn't exclude it. Patients with clear peritoneal signs go straight to surgery; for others, angiography or CT angiography is the diagnostic test of choice.

Liver failure and encephalopathy at the bedside

MSD's acute liver failure chapter (full review August 2025) defines it as liver failure lasting under 26 weeks in a patient without prior liver disease, with encephalopathy and coagulopathy; an INR above 1.5 with altered sensorium usually confirms it. Points that matter at the bedside:

• Don't assume the confusion is encephalopathy. MSD says worsening mental status calls for head CT to look for cerebral edema and often bedside glucose testing, because cerebral edema is common with severe encephalopathy and hypoglycemia can occur.
• A high INR isn't the whole story. Bleeding is rare unless DIC is present, because pro- and anticoagulant factors are rebalanced, and these patients may even be hypercoagulable.
• Infection hides. Respiratory and urinary infections and sepsis are common, and localizing symptoms may be absent.

In chronic liver disease, MSD's portosystemic encephalopathy chapter lists the usual precipitants: GI bleeding, infection, electrolyte imbalance (especially hypokalemia), dehydration, diuretics, and sedatives, alcohol or analgesics. Treatment corrects the trigger and clears the bowel, most often with lactulose titrated to 2 or 3 soft stools a day, sometimes with rifaximin; MSD says protein restriction isn't necessary. Asterixis, the flapping tremor with outstretched, dorsiflexed wrists, is the sign to look for.

Intra-abdominal pressure: measure it right, then grade it

This section follows the 2013 World Society of the Abdominal Compartment Syndrome (WSACS) consensus guidelines (Kirkpatrick and colleagues, Intensive Care Medicine). Their measurement standard:

• Method. The bladder is the reference standard for intermittent measurement, with a maximal instillation volume of 25 mL of sterile saline.
• Conditions. IAP is expressed in mm Hg and measured at end-expiration, supine, after making sure abdominal muscle contractions are absent, with the transducer zeroed at the midaxillary line.
• Normal. About 5 to 7 mm Hg in critically ill adults.

And their definitions:

Worked example (fictional; arithmetic is Passy's). After an emergency laparotomy and a large-volume resuscitation, a ventilated patient's bladder pressures read 21, 22 and then 23 mm Hg over six hours while urine output falls below 0.5 mL/kg/h. The MAP is 74 mm Hg. A pressure that stays above 20 with new kidney dysfunction meets the ACS definition, and APP = 74 − 23 = 51 mm Hg. The nursing step is to report the trend with the organ dysfunction, recheck that each reading followed the measurement rules, and prepare for the team's response.

What WSACS says about management: it recommends measuring IAP when any risk factor for IAH or ACS is present in a critically ill or injured patient, protocolized monitoring and management, efforts to avoid sustained IAH, and decompressive laparotomy for overt ACS. It suggests optimal pain and anxiety relief, brief trials of neuromuscular blockade as a temporizing measure, considering body position, nasogastric or rectal decompression when the stomach or colon is dilated, and a protocol to avoid a positive cumulative fluid balance once acute resuscitation is complete. For an open abdomen, it recommends negative pressure wound therapy, which links this topic to the wound VACs the test plan lists. Once the measurement rules feel automatic, test the bladder pressure technique item in the free CCRN set, and when you want a tougher mix, Hard Mode challenges are planned for CCRN prep.

AKI by KDIGO 2012: the definition and the urine-output arithmetic

KDIGO's 2012 guideline defines acute kidney injury as any of: a rise in serum creatinine of at least 0.3 mg/dL within 48 hours; a rise to at least 1.5 times baseline known or presumed to have occurred within 7 days; or urine output below 0.5 mL/kg/h for 6 hours. It stages severity as follows:

Worked example (fictional; arithmetic is Passy's). An 80-kg patient's creatinine rises from 0.9 to 1.4 mg/dL over 30 hours. The rise of 0.5 mg/dL within 48 hours meets the definition, and 1.4 ÷ 0.9 ≈ 1.6 times baseline is Stage 1. For urine output, 0.5 mL/kg/h × 80 kg = 40 mL/h: below 40 mL/h for 6 to 12 hours is Stage 1, for 12 hours or more Stage 2. The Stage 3 line is 0.3 × 80 = 24 mL/h for 24 hours. KDIGO stages by whichever criterion gives the higher stage, so an hourly urine total is as important as the morning creatinine. Staging thresholds like these suit the planned CCRN flashcard deck.

Treatment statements from KDIGO 2012 worth knowing:

• Fluids and pressors. Absent hemorrhagic shock, it suggests isotonic crystalloids rather than colloids for initial volume expansion (2B), and recommends vasopressors with fluids in vasomotor shock (1C).
• Diuretics. It recommends not using diuretics to prevent AKI (1B) and suggests not using them to treat AKI except to manage volume overload (2C).
• Dopamine. It recommends not using low-dose dopamine to prevent or treat AKI (1A).

A date to watch. KDIGO's AKI guideline page says a draft 2026 Clinical Practice Guideline for AKI and acute kidney disease has been released for public review, with revised definitions that add structural biomarkers to functional criteria. It hadn't been published when this page was checked, so the 2012 definitions above remain the published ones; recheck before you test.

Nephrotoxins the CCRN expects you to spot

"Identify nephrotoxic agents" is a testable nursing action. The sources name these:

• Aminoglycosides. KDIGO suggests not using them for infections unless no suitable, less nephrotoxic alternative is available (2A), recommends drug-level monitoring with multiple daily dosing beyond 24 hours (1A), and suggests single daily dosing in patients with normal, stable kidney function (2B).
• Amphotericin B. KDIGO suggests lipid formulations over conventional amphotericin (2A), and recommends azoles or echinocandins over conventional amphotericin when equally effective (1A).
• Iodinated contrast. KDIGO recommends IV volume expansion with isotonic sodium chloride or sodium bicarbonate rather than none in patients at increased risk (1A), and not relying on oral fluids alone (1C).
• Others in MSD's AKI chapter. Vancomycin and aminoglycosides as causes of nephrotoxic tubular injury, endogenous pigments such as myoglobin from rhabdomyolysis and hemoglobin from hemolysis, and NSAIDs among the drugs that can cause kidney injury.

The free CCRN set has an item that asks which new order to question first in a septic patient whose creatinine is rising; check your nephrotoxin call in the free CCRN questions after this list.

CRRT, intermittent dialysis and anticoagulation: what KDIGO suggests

MSD's AKI chapter (full review February 2026) calls hyperkalemia and pulmonary edema the most serious complications of AKI, and lists dialysis as needed to control hyperkalemia, pulmonary edema, metabolic acidosis and uremic symptoms. KDIGO's position on the modality:

• Complementary, not rival. It says continuous and intermittent RRT should be used as complementary therapies (not graded).
• CRRT for instability. It suggests CRRT rather than standard intermittent RRT for hemodynamically unstable patients (2B), and for AKI patients with acute brain injury or raised intracranial pressure (2B).
• Citrate for CRRT. For patients without increased bleeding risk, it suggests regional citrate anticoagulation rather than heparin during CRRT when citrate isn't contraindicated (2B).
• Timing by context. It says the decision to start RRT should weigh the clinical context and trends rather than single BUN and creatinine thresholds, and that RRT should start emergently for life-threatening fluid, electrolyte or acid-base changes.

Skin on the CCRN: necrotizing infection, pressure injury and the listed devices

Necrotizing soft-tissue infection. MSD's chapter (full review May 2026) describes tissue that looks like severe cellulitis, warm, red or violaceous and swollen, with pain out of proportion to the clinical findings. Bullae, crepitus from tissue gas and gangrene may follow. The diagnosis is primarily clinical, surgical exploration is the gold standard, and MSD warns that treatment shouldn't be delayed while waiting for CT or MRI. One meta-analysis it cites put global mortality at 23.1%. For the nurse, a cellulitis that hurts far more than it looks, or changes color quickly, is reported now.

Pressure injury. Prevention and staging are testable. The published PCCN multisystem review has a stage-by-stage table from the MSD Manual that applies equally to ICU patients.

IV infiltration. The test plan lists it and its treatment, but this review doesn't cover it; AACN's bibliography includes the Infusion Nurses Society's Infusion Therapy Standards of Practice (9th edition, 2024).

Your next step for CCRN GI, renal and skin

Practice the two calculations in this guide on your own patients this week: an APP from a real bladder pressure and MAP, and a KDIGO stage from a real creatinine trend and hourly urine. Then read the hematology and immunology review for the rest of Category C, and the multisystem emergencies review for rhabdomyolysis, which links muscle injury to the kidney.