NGN Case Study Practice Questions

Lipase greater than three times the upper limit of normal (1,480 U/L against a ceiling of 82) is the diagnostic anchor for acute pancreatitis, though the degree of elevation does not predict severity. Temperature 38.2 C and heart rate 118/min together signal the systemic inflammatory response that drives early pancreatitis mortality; meeting two or more SIRS criteria on admission predicts a more severe course and demands closer monitoring than a routine medical admission. A hematocrit of 47% against a documented baseline of 39% is hemoconcentration from third-spacing of plasma into the retroperitoneum — an early, easily missed marker of intravascular volume depletion and a recognized predictor of persistent organ failure. A respiratory rate of 24/min with shallow splinted breathing is not merely a pain response: pancreatitis causes diaphragmatic irritation, atelectasis, and pleural effusion, and a rising respiratory rate is the earliest sign of the pulmonary complications that follow.

SpO2 of 95% on room air is within normal limits and is not itself an immediate concern, though it must be trended alongside the respiratory rate. Triglycerides of 140 mg/dL are normal; they are checked because levels above 1,000 mg/dL cause pancreatitis, so this value effectively rules that etiology out rather than raising a concern. Creatinine of 1.1 mg/dL sits at the upper limit of normal and, without a rising trend, does not yet demonstrate acute kidney injury — the BUN elevation is the more sensitive early volume marker here. Recognizing cues means separating findings that are abnormal and clinically meaningful from those that are simply present in the chart.

Analyzing cues means grouping findings by the mechanism that produced them. Hemoconcentration (hematocrit 39% to 47%) with BUN 24 mg/dL against a high-normal creatinine of 1.1 mg/dL is a BUN:creatinine ratio near 22:1 — a prerenal pattern from plasma loss into the inflamed retroperitoneum plus vomiting. The same mechanism explains tachycardia, a systolic pressure 34 points below the client's own baseline, and oliguria at 20 mL/hr, well under the 0.5 mL/kg/hr goal for a 92 kg client (46 mL/hr). This cluster drives goal-directed isotonic crystalloid resuscitation, preferably lactated Ringer's.

Hyperbilirubinemia with scleral icterus, an elevated alkaline phosphatase, and an ALT of 210 U/L point to a stone obstructing the common bile duct, the etiology of this pancreatitis. An ALT above roughly 150 U/L early in the attack is one of the most useful biochemical clues to gallstone origin. This cluster drives ERCP and index-admission cholecystectomy decisions, not the fluid plan.

Fever with leukocytosis and elevated CRP reflects the typically sterile, cytokine-mediated inflammatory response of pancreatic autodigestion. CRP peaks at 48 to 72 hours; values above roughly 150 mg/L correlate with necrosis, so it is trended rather than acted on once. Because this client also has obstructive jaundice, ascending cholangitis must be actively excluded — fever plus jaundice plus right upper quadrant pain is Charcot's triad, and if cholangitis is present, antibiotics and urgent ERCP within 24 hours ARE indicated. Absent that documented infection, current US guidance (ACG) is explicit that prophylactic antibiotics are not indicated in acute pancreatitis, including necrotizing disease. The common error is either reflexively treating early SIRS as infection, or dismissing fever in a jaundiced client before cholangitis has been ruled out.

Acute respiratory distress syndrome is a well-recognized complication of severe acute pancreatitis and a leading cause of early death. The diagnostic picture is present in full: acute onset within one week of a known insult, bilateral infiltrates on chest imaging, hypoxemia not explained by cardiac failure or volume overload, and a PaO2/FiO2 ratio in the moderate range. At 4 L nasal cannula the estimated FiO2 is about 0.36, so 56 divided by 0.36 yields roughly 155 — moderate ARDS. The respiratory alkalosis (pH 7.47, PaCO2 30) is compensatory hyperventilation that precedes decompensation; when the PaCO2 begins to normalize or rise in a client breathing 30 times a minute, that is fatigue, not improvement.

Cardiogenic pulmonary edema is the distractor that punishes surface reasoning: the client did receive fluid, and crackles are present. But flat jugular veins, no S3, no edema, a normal cardiac silhouette, and ongoing oliguria with hypotension all indicate she remains intravascularly depleted. Diuresing her here would worsen perfusion and kidney injury. Aspiration pneumonia is plausible after repeated vomiting but typically produces focal, often right-sided infiltrates rather than diffuse bilateral opacities in this time frame. Atelectasis does not produce a P/F ratio of 155 or diffuse bilateral infiltrates.

The incorrect evidence choices are all true statements about this client, which is exactly the trap. Lipase, fever, and abdominal findings support the diagnosis of pancreatitis; only the oxygenation and imaging data support the specific hypothesis of ARDS.

Oxygenation is the immediate priority. Titrating to an SpO2 of 92% to 96% and anticipating escalation to high-flow nasal cannula, noninvasive ventilation, or intubation is appropriate for moderate ARDS with a respiratory rate of 30; anticipating that escalation is what separates a prepared nurse from a reactive one. Fluid resuscitation continues because this client is still volume depleted, but it is goal-directed and moderate — current US guidance favors lactated Ringer's at a moderate rate titrated to clinical targets over the historical aggressive-bolus approach, which increased fluid overload without improving outcomes. Head-of-bed elevation reduces diaphragmatic splinting from a distended abdomen and lowers aspiration risk. Adequate analgesia is a respiratory intervention here: a client splinting from severe pain cannot expand her lung bases, and there is no evidence that opioids worsen pancreatitis outcomes.

Continuous monitoring with serial ABGs is how the nurse detects the transition from compensated hyperventilation to respiratory failure before it becomes an emergency. Early enteral nutrition, begun within 24 to 48 hours once hemodynamics allow, preserves gut mucosal integrity and reduces infectious complications compared with prolonged bowel rest or parenteral nutrition.

Furosemide is wrong: the infiltrates reflect inflammatory capillary leak, not volume overload, and diuresis in a hypotensive, oliguric client accelerates acute kidney injury. Prophylactic antibiotics are wrong: fever, leukocytosis, and elevated CRP in the first 72 hours reflect sterile inflammation, and prophylaxis has not been shown to reduce mortality or infected necrosis while it does select for resistant organisms and fungal superinfection. Antibiotics wait for documented or strongly suspected infection.

Hypocalcemia in acute pancreatitis results from saponification — released lipase digests peritoneal fat and the free fatty acids bind calcium — compounded here by hypomagnesemia and hypoalbuminemia. An ionized calcium of 0.98 mmol/L with perioral paresthesia and a positive Chvostek sign is symptomatic hypocalcemia and warrants IV calcium gluconate, given slowly through a patent line with cardiac monitoring. Ionized calcium, not total calcium, is the value to trust when albumin is 2.8 g/dL.

Magnesium must be corrected for the other electrolytes to correct. Hypomagnesemia both causes refractory hypocalcemia — it impairs parathyroid hormone release and end-organ response — and drives renal potassium wasting, so replacing potassium at 3.2 mEq/L without addressing a magnesium of 1.4 mg/dL will fail. Continuous cardiac monitoring is indicated because hypocalcemia prolongs the QT interval, and hypokalemia with hypomagnesemia predisposes to torsades de pointes.

Pain at 7/10 on PRN dosing represents a failed analgesic plan; scheduled or patient-controlled analgesia should be requested, since uncontrolled pain perpetuates splinting, atelectasis, and catecholamine-driven tachycardia.

Withholding opioids to avoid masking the abdomen is outdated reasoning. Diagnosis here rests on imaging and laboratory trends, and analgesia does not obscure the deterioration that matters. Routine nasogastric suction is likewise obsolete: it is reserved for intractable vomiting or ileus and offers no benefit, only added discomfort, for clients without those problems. This client is not vomiting.

Evaluating outcomes means judging each finding against where the client started, not against a textbook normal.

Oxygenation has improved: her SpO2 fell to 88% on room air at hour 6 (P/F ratio approximately 155 on 4 L nasal cannula) and she then required high-flow nasal cannula, and she is now 96% on 2 L with a respiratory rate of 20 — the acute lung injury is resolving. Urine output has improved from 0.15 mL/kg/hr to 0.8 mL/kg/hr, exceeding the 0.5 mL/kg/hr resuscitation target; with an improved blood pressure and a heart rate down from 126, this reflects successful volume restoration. Ionized calcium has risen from 0.98 to 1.14 mmol/L, at or near the lower limit of normal (reference ranges are lab-dependent, roughly 1.12-1.30 mmol/L), and potassium and magnesium are now normal — the electrolyte plan is working. The keyed direction depends on the trend, not on which lab's cutoff is used.

Two findings have worsened and belong together. A new fever after 36 afebrile hours with WBC climbing from 14,000 to 21,000 warrants evaluation for secondary infection — line, urinary, pulmonary, or biliary sources, and, though uncommon this early, infected necrosis, which typically develops after the second week. New palpable epigastric fullness with escalating pain and distention suggests an evolving acute peripancreatic fluid collection or acute necrotic collection (per the revised Atlanta classification, pseudocyst and walled-off necrosis require more than 4 weeks to mature). This is exactly why contrast-enhanced CT is pending.

Glucose of 190 mg/dL is unchanged from 24 hours ago. It remains abnormal and needs continued insulin titration, but there is no movement in either direction. Students often mark any abnormal value "worsened"; evaluation asks for direction of change, not simple normality.