A 45 year-old female with a history of pre-diabetes and gastroesophageal reflux disease presents with 3 days of epigastric abdominal pain. She describes constant, burning abdominal pain which worsened on the day of presentation associated with two episodes of non-bloody and non-bilious emesis. The patient was tender to palpation in the epigastrium and right upper quadrant.

Laboratory studies were largely normal. A complete blood count demonstrated minimal leukocytosis (11.6 with normal differential), and liver function tests were normal.

A right-upper quadrant ultrasound was obtained which demonstrated “strongly shadowing structures in the gallbladder fossa which might represent a wall-echo-shadow, calcified gallbladder wall, or air within the gallbladder”.

The patient underwent contrast-enhanced computed tomography of the abdomen and pelvis which is shown below.

Imaging

The patient was taken to the operating room for exploratory laparotomy, possible cholecystectomy and possible small bowel resection for presumed gallstone ileus. Intra-operative findings were notable for a cholecystogastric fistula which was repaired.

Differentiation between Portal Venous Gas and Pneumobilia

The patient’s CT demonstrated mostly central hepatic gas. This finding combined with the presence of an air-fluid level in the gallbladder was most consistent with pneumobilia. This case demonstrates an application of the previously-developed algorithm for the evaluation of hepatic gas in a relatively unique pathologic process.

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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

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:

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

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

Evaluation of AKI: ⁴

References:

1. 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
2. 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
3. Lameire, N., Van Biesen, W., & Vanholder, R. (2005). Acute renal failure. Lancet, 365(9457), 417–430. doi:10.1016/S0140-6736(05)17831-3
4. Thadhani, R., Pascual, M., & Bonventre, J. V. (1996). Acute renal failure. New England Journal of Medicine, 334(22), 1448–1460. doi:10.1056/NEJM199605303342207
5. WikEM: Acute kidney injury

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Consultation for bowel obstruction

HPI:

The patient is a 40yo male with a history of alcohol abuse, and seizure disorder secondary to traumatic brain injury who was admitted to this hospital 4d ago after an altercation with law enforcement officials. On arrival, the patient was reported to be acutely intoxicated with ecchymosis and bleeding from left lateral/posterior head and ear. No other significant injuries were found and the patient underwent CT imaging of head and c-spine, with notable findings of left occipital epidural hematoma, subarachnoid hemorrhage, but no significant midline shift. Neurosurgery was consulted and no emergent surgical intervention was required, the patient underwent serial imaging to monitor the bleed which was found to be stable and the patient slowly returned to baseline mental status.

On HOD4, the patient developed nausea/vomiting and abdominal pain, a nasogastric tube was placed with feculent output. CT abdomen/pelvis showed high grade SBO and possible mesenteric ischemia/infarct, and general surgery was consulted for further evaluation. The patient reported experiencing some abdominal pain since the altercation, but could not recall if he was hit in the abdomen.

PMH:

• Alcohol abuse
• Seizure disorder

PSH:

• Tibia fracture
• No prior abdominal surgery

FH:

• Non-contributory

SHx:

• Current alcohol, marijuana use, no tobacco use
• History of homelessness

Medications:

• Norco PRN
• Ativan PRN
• LISS, SQH, Thiamine
• NKDA

Physical Exam:

• VS:  T 99.5°F    HR 108    RR 16    BP 128/82    O2 99% RA
• Gen: NAD
• HEENT: PERRL, EOMI, sclera clear, anicteric
• CV: RRR, normal S1/S2
• Lungs: CTAB
• Abd: Distended, diffuse tenderness to palpation, no rebound tenderness, no ecchymoses or signs of trauma
• Ext: Warm, well-perfused
• Neuro: AAOx4, appropriate

Assessment/Plan:

40M w/hx alcohol abuse, TBI and seizure disorder, presented initially with evidence of head trauma which was stabilized. However, the development of abdominal pain, N/V, and finding of distension on exam associated with copious output of feculent material from NGT suggests bowel obstruction. This patient has no history of abdominal surgeries to suggest adhesions as a possible cause. Though the patient cannot recall any abdominal trauma, and there was no e/o trauma on exam, findings on CT abdomen/pelvis are suggestive of traumatic cause (hematoma causing obstruction or ischemia resulting from mesenteric injury). The patient was monitored for several days, continuing NGT to suction and with serial abdominal films. However, abdominal pain persisted, abdominal radiographs showed worsening obstruction and the patient developed leukocytosis and on HOD7 the patient was taken to the OR for exploratory laparotomy. Upon entering the peritoneal cavity, there was obvious blood and very distended small bowel which was run distally with finding of a mesenteric laceration in the distal ileum which was walled off by omentum. Additionally, a grade 2 splenic laceration was found. Ultimately, a small bowel resection with primary anastomosis along with a repair of the splenic laceration was performed.

Imaging:

CT abdomen/pelvis

Moderate abdominal and pelvic ascites which has Hounsfield unit attenuation is greater than simple fluid suggestive of blood products.

CT abdomen/pelvis

Fluid dilated small bowel

CT abdomen/pelvis

Complex transition point in the central mid abdomen.
Segment of bowel at the transition point has circumferential mural thickening and surrounding complex attenuation mesenteric fluid and mesenteric stranding.

Abdominal X-Ray

Small bowel distention
Nasogastric tube is seen coiled in the gastric fundus

CT Head

Left occipital extracranial soft tissue hematoma
Left occipital epidural hematoma subjacent to the fracture site in addition to subarachnoid hemorrhage within the sulci of the left temporal lobe and interpeduncular cistern
Extra-axial fluid collection along the right frontal convexity, tracking down the anterior falx, compatible with a subdural hematoma

Differential Diagnosis for bowel obstruction: ^{1, 2, 3}

Types of Abdominal Pain: ⁴

References:

1. Kulaylat MN, Doerr RJ. Small bowel obstruction. In: Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001. Available from: http://www.ncbi.nlm.nih.gov/books/NBK6873/
2. Jackson, P. G., & Raiji, M. T. (2011). Evaluation and management of intestinal obstruction. American family physician, 83(2), 159–165.
3. Maung, A. A., Johnson, D. C., Piper, G. L., Barbosa, R. R., Rowell, S. E., Bokhari, F., Collins, J. N., et al. (2012). Evaluation and management of small-bowel obstruction. Journal of Trauma and Acute Care Surgery, 73, S362–S369. doi:10.1097/TA.0b013e31827019de
4. Stabile, Bruce. “The Acute Abdomen.” Chairman’s Hour. Harbor UCLA Department of Surgery Student Lecture Series. 5/17/13. Lecture.

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