This document presents the case of a 70-year-old woman admitted to the ICU with hypotension, hypoxia, abdominal tenderness and distension. She developed intra-abdominal hypertension with an intra-abdominal pressure of 26 mmHg. Imaging revealed occlusion of the superior mesenteric artery near its origin with infarction of the right kidney and spleen. Her condition was too poor for surgery, so medical management was initiated for her intra-abdominal hypertension and multiple organ dysfunction.

2. Case presentation
By Dr.Ahmed ElMaghraby
IMC-ICU Specialist
5-3-2013

3. BACKGROUND:
A 70-year-old woman with known history of DM, HTN,
CAD,ICM with EF:30%, was recently treated in the CCU
for pulmonary congestion, which improved with lasix.
On the day of discharge, She developed ↓↓ K then afib.
with a rapid ventricular response. She was HD stable,
She was reverted to NSR within 24hrs after K was
corrected and received amiodarone.
She received only prophylactic anticoagulation as she
had BPR with mild abd. Pain soon after she developed
AFIB, which was diagnosed by surgeon as bleeding
hemorrhoids.
All labs. Was unremarkable except for ↓↓ K.

4. Admission to ICU
Next day, she began to have LOC, agitation with no
lateralization, neuro. Cons. Added haloperidol as she
didn’t sleep for 2days.
She had low grade fever, with no apparent site of
infection.
She began to desaturate on room air requiring FM with
high flow, then BIPAP mask, with progressive
hypotension.
Intensivests were consulted, ABG revealed hypoxia with
combined resp. and metabolic acidosis.
Examination revealed GCS 7/15, ↓↓BP, ↓↓temp, ↑↑HR,
↑↑RR, bil. coarse creps., distended abdomen, peripheral
pulsation not palpable, severe hypoxia.
She was intubated, MV ,she became bradycardic, coded
successful CPR after 5min..

5. In the ICU
On physical examination, the patient was intubated ,
MV. She was hypotensive, with a blood pressure of
60/30 mm Hg, and tachycardic, with a heart rate of 180
bpm. hypothermic(temperature, 35°C). Her oxygen
saturation is 85 on FIO2 100%.
Her head, neck examinations were all normal. The heart
rate is rapid and periodically irregular, with jugular
venous distention but no peripheral edema is detected.
She had abdominal wall distension & tenderness.
The abdomen is firm and diffusely tender to palpation,
without rebound or guarding, and hypoactive bowel
sounds are noted.
On neurologic examination, she localized to pain, no
lateralization, pupils dil. reactive., eye opening to pain.

6. CBC and metabolic panel reveal leucocytosis (28.1 ),
anemia (hg 7.3 gm/dL, ht 21.1 %),thrombocytopenia(50)
hyperkalemia (5.9 mmol/L), renal imp. (creat. 1.6 mg/dL,
(BUN) 32 mg/dL, and an anion gap met. acidosis
(carbon dioxide 10 mmol/L, anion gap 23 mEq/L).
Elevated LFT, with an (ALT) of 73 IU/L, and an (AST)
129 IU/L. Her (PT) is 18.2, correlating with an (INR) of 2.
The cardiac enzymes include a total creatinine kinase
(CK) of 21 IU/L, CK-MB 1.8 ng/mL, and troponin of 0.19
ng/mL. Electrocardiography (ECG) shows afib with a
rapid ventricular response, but no evidence of acute
ischemia. Lactate of 9 mmol/l. mildly elevated lipase ,&
elevated amylase.
Chest x ray: bil. Infiltrates.

7. Problem list:
HTN,DM
CAD,ICM
Paroxysmal afib
DCL
Acute Resp.fail.
Acute renal fail.
Severe sepsis ,septic shock
MOSF
Abdominal tenderness., BPR
Anemia, Thrombocytopenia, coagulopathy.
Severe metabolic, lactic acidosis, high AG

16. The patient was anuric with distended
tender abdomen.
IAP was 26 mmhg.
ABD. X ray supine done: gases with no air
fluid level, no air under diaphram.
Abd us :distended bowel loobs mild free
ascites

17. Intra-abdominal hypertension (IAH)
Normal IAP is thought to be around 5 mmHg.
Defined by IAP >12 mmHg. IAH can be graded as:
Grade I. IAH: IAP between 12-15 mmHg
Grade II. IAH: IAP between 16-20 mmHg
Grade III. IAH: IAP between 21-25 mmHg
Grade IV. IAH: IAP >25 mmHg
Abdominal compartment syndrome (ACS) is defined by a
sustained increase in IAP above 20 mmHg in association
with new onset single or multiple organ system failure. In
contrast to IAH, ACS is not graded, but rather
considered as an 'all or nothing' phenomenon.

18. Causes of IAH:

19. Medical treatment:
1. Improvement of abdominal wall compliance: Sedation, Neuromuscular
blockade
2. Evacuation of intra-luminal contents: Gastric tube and suctioning,
Gastroprokinetics (erythromycin, metoclopramide), Rectal tube and
enemas, Colonoprokinetics (neostigmine, prostygmine bolus or infusion),
Endoscopic decompression of large bowel
3. Evacuation of peri-intestinal and abdominal fluids
4. Correction of capillary leak and positive fluid balance: Albumin in
combination with diuretics , Dialysis or ultrafiltration
5. Specific therapeutic interventions
Continuous negative abdominal pressure (CNAP)
Negative external abdominal pressure (NEXAP)
Targeted abdominal perfusion pressure (APP)

20. Indication for surgery
If IAP continues to increase and organ function further
deteriorates after initiation of medical treatment, consider
surgical decompression in all patients with ACS.
Decompressive laparotomy is the only definite treatment
available today for ACS. It results in a prompt decrease
in IAP in the majority of patients, although in most of
them IAP remains above 12 mmHg, and in some
patients some degree of organ dysfunction may persist.
Timing of the procedure, the degree of pre-existing
organ dysfunction and its evolution are possible factors
affecting outcome in patients with ACS.

22. Ct abd with oral and IV contrast done
revealed occlusion in SMA near origin ,
occluded rt. renal artery and splenic artery
with renal and splenic infarction.
surgery cons. But general condition was
very poor for surgery

23. THANK YOU