Small Bowel Obstruction

Paige L BakerOctober 4, 2006

H&P

CC: “My stomach hurts and I’ve been vomiting for the past 5 days”

HPI: 59 y/o HM recently admitted on 9/19/06 for abdominal pain, vomiting and diarrhea which resolved after 24 hours and pt was discharged. Upon discharge, he was well until the evening when he began to experience abdominal pain most prominent in the LUQ and LLQ.

HPI Cont:

He describes this pain as crampy in character, continuous, 8 out of 10 on the pain scale and non-radiating. Vomiting temporarily relieves the pain, but the pain reoccurs a short while later. He also states that eating worsens the pain and that he has not eaten for the past five days as a result. This is the first time he has experienced abdominal pain such as this.

HPI Cont:

After the onset of the abdominal pain, the pt began vomiting approximately once every two hours. He described it as dark brown in color, foul-smelling and minimal in amount. He states that he has not had a bowel movement or passed flatus since discharge five days ago.

HPI Cont:

Since the onset of symptoms, he has also been experiencing progressive generalized weakness, dizziness and lightheadedness. He was then brought in by EMS due to worsening of symptoms.

PMHx:

DM, HIV dx in 1996 (last CD4 count was ~900 per pt) on HAART, schizophrenia, arthritis, polysubstance abuse

PSHx: S/p small bowel resection and colostomy in 1989 for colonic perforation. S/p colostomy reversal 1998.

Medications at Home:

Risperdol 1mg bid, depakote 500mg bid, combavir, invarase, motrin 600mg q6. Previously on Naproxen 375 mg bid and metformin, recently stopped taking.

Allergies: NKDA

Family Hx:

Mother dx with HTN and DM ~ 10 years ago. Maternal uncle died of laryngeal ca at 55 yoa. Sister dx with DM at 51 yoa.

Social Hx:

Pt currently unemployed and living in a shelter. Smokes 1 ppd since the age of 13 (46 pack-year hx), drinks 2-3 beers per week and last used heroin 1 week ago. No recent travel. Last PPD negative six weeks ago.

ROS:

General: 2-3 lb recent weight loss, +fatigue, +weakness, -fever, -chills, -night sweats.

Skin: -skin/hair/nail changes, - rashes, -itching HEENT: -trauma, -headache, -visual or auditory

changes, -tinnitus, -discharge, -earache, -rhinorrhea, -epistaxis,-hoarsness, -sore throat, -dysphagia/odynophagia,

Respiratory: -SOB, -cough, -wheezing, -hemoptysis, Cardiac: -palpitations, -chest pain, -DOE, -PND, -

edema, -orthopnea

ROS:

GI: +anorexia, +nausea, +vomiting, +constipation, +obstipation, -diarrhea, +abdominal pain, -jaundice

GU: -frequency, -urgency, -polyuria, -dysuria, -hematuria, -nocturia, -incontinence, -penile discharge/sores, -testicular pain or masses

Vacular: -leg edema, -claudication, Musculoskeletal: +joint stiffness, +joint pain, -

decrease range of motion Neurologic: - loss of sensation/numbness, -tingling, -

tremors, -weakness/paralysis, -fainting/blackouts, -seizures

ROS:

Hematologic: -easy bruising/bleeding, -petechiae, -purpura, -transfusions

Endocrine: -heat/cold intolerance, -excessive sweating

PE:

VS in ER BP 140/90 PR 98/min RR 16/min Tc 98.5o

spO2 99% on room air.

AAO x 3, in mild distress due to pain Skin: dry, + tenting HEENT: PERRLA, EOMI, + dry buccal mucosa, -

thyromegally, -cervical lymphadenopathy, Neck: supple, -JVD, prominent R external jugular vein Cardiac: S1 S2 NRR, no M/R/G

PE Cont:

Pulmonary: CTA b/l, no wheezes, good air entry b/l

Abdominal: midline scar, +ventral hernia with palpable small bowel, +enterocutaneous fistula LLQ, Soft, ND, +BS, + tenderness in all quadrants, most prominent in LUQ and LLQ, -rebound, + voluntary guarding, - shifting dullness, -CVA tenderness, -Hepatosplenomegally

PE cont:

Extremities/Vascular: No edema or cyanosis. Pulses equal throughout

Rectal: stool present in rectal vault, -guiaic, no masses

Musculoskeletal: FROM, - muscle atrophy Neurologic: CN II-XII intact, -sensory or motor

deficits, 2+ reflexes in upper and lower extremities, normal gait.

Labs:

19

35.543812.4

126

4.0

84

22.9

90

1.5

164

8.6

2.4

Labs Cont:

LFT’s: 24/44/136/0.52/0.25/8.8/3.5 Amylase 76 Lipase 180

129

3.6

89

22.9

83

1.3

138

7.8

Labs Cont:

EKG: sinus tachycardia at 103 BPM, non-specific t wave changes

CXR: No infiltrates, masses, edema or effusions

Abdominal x-ray: dilated small bowel loops with air fluid levels, -perforation, -free air

CT scan

A&P

59 y/o HM with PMHx or DM, HIV, Schizophrenia, Polysubstance abuse, S/p small bowel resection and colostomy for perforation. S/p colostomy reversal, admitted for likely SBO, enterocutaneous fistula and hyponatremia.

A&P Cont:

-NPO/IV hydration D5NS at 200cc/hr -NGT decompression -Morphine 2mg/IM q4hr for pain -Reglan 10mg/IV q6hr prn, Pepcid 20 mg IV qd -Monitor BMP, lactate, serum ketones,VBG, UA, FS,

urine electrolytes Foley catheter placement for strict I&O measurement

Small Bowel Obstruction

What is SBO? Mechanical obstruction to the passage of intraluminal contents

In the US, SBO accounts for up to 20% of all acute surgical admissions

SBO Pathophysiology

Obstruction leads to proximal dilation due to the accumulation of GI secretions and swallowed air.

Dilation stimulates secretory activity and peristalisis both above and below the level of obstruction

This leads to frequent loose stools and flatulence early in the course of an SBO.

SBO Pathophysiology Cont.

Vomiting occurs if obstruction is proximal.

Distention can compress mucosal lymphatics resulting in bowel wall lymphedema/ third spacing of fluid and dehydration/electrolyte loss

SBO Pathophysiology Cont

• Bacteria in the gut proliferate proximal to the obstruction.

• Microvascular changes in the bowel wall allow translocation to the mesenteric lymph nodes

• This is associated with an increase in incidence of bacteremia due to Escherichia Coli in patients with SBO.

SBO Signs and Sx

Abdominal discomfort/pain, cramping, nausea, vomiting and abdominal distention.

Hyperactive bowel sounds and diarrhea/flatulence occur early

Constipation/Obstipation and hypoactive bowel sounds occur late and may indicate complete obstruction.

What causes SBO?

Post operative adhesions, hernias, tumors, Chron’s disease, intussusception, volvulus, gallstone ileus, bezoars, abscesses, diverticulitis, bowel wall hematoma (coumadin),annular pancreas, Meckel’s diverticulum, SMA syndrome

What causes SBO cont:

Postsurgical adhesions are the most common cause of SBO

May cause acute obstruction within four weeks of surgery or decades later

The incidence of SBO parallels the increasing number of laparotomies performed in developing countries.

Common Surgeries & SBO

In the US, appendectomy is most commonly associated with SBO, followed by; colorectal, gynecological, GI surgeries and herniorrhaphy.

Lower abdominal and pelvic surgeries lead to obstruction more often than upper GI surgeries

Signs/Sx of Strangulated SBO

Fever, tachycardia, severe/continuous pain, hematemesis, shock, pneumatosis intestinalis, gas in portal vein, pneumoperitoneum, peritoneal signs, acidosis (lactic acidosis) and gross or occult blood.

Always a surgical emergency.

Incomplete SBO Tx:

Incomplete SBO Tx? Initally, conservative treatment (NPO, NGT decompression, IVF, Foley) and close observation

Complete SBO Tx:

Complete SBO Tx? Exploratory laparotomy with possible bowel resection and lysis of adhesions (LOA)

Absolute Surgical Indications

Peritoneal signs or free air on AXR are absolute indications for surgery.

Strangulated obstructions are always surgical emergencies.

Mortality/Morbidity

Dependent on early recognition and dx of obstruction

If untreated, strangulated obstructions cause death in 100% of patients

Morbidity/Mortality Cont

If surgery is performed within 36 hours, the mortality decreases to 8%

The mortality rate approaches 25% if surgery is extended beyond 36 hours.

Article:

Nonsurgical Management of Partial Adhesive Small-bowel Obstruction with oral therapy: a randomized controlled

trial.

Shyr-Chyr Chen, Zui-Shen Yen, et al.

CMAJ • November 8, 2005; 173 (10).

Background

Pts with partial SBO due to adhesions are initially managed conservatively with NGT decompression, NPO and IVF hydration.

This management is reported to be successful in 73%-90% of cases

However, this approach may result in longer hospital stays (usually between 1-3 weeks) increased hospital costs and increased risks of delayed surgery (ie strangulation if >48 hours)

Will addition of oral laxative, digestant and defoaming agent to traditional therapy shorten length of hospital stay and decrease frequency of subsequent surgical intervention?

Methods

144 patients admitted between Feb 2000-July 2001 to tertiary care hospital in Taipei

Only included patients with partial SBO due to adhesions

Control group received NGT decompression Tx, IVF and NPO

Intervention group received the same tx as the control group in addition to 500 mg Mg oxide tid, 0.3g Lactobacillus acidophilus tid and 40 mg simethicone tid.

Attending surgeon regularly assessed the patients condition and was blinded to the treatment modality

Methods Cont;

Surgical intervention in both groups was determined by the attending surgeon based on the presence of one or more toxic signs (eg. Fever, leukocytosis, intractable pain and peritonitis) or if the obstruction did not resolve spontaneously within five days.

Results

The number of patients whose obstruction was successfully tx without surgery was significantly higher in the intervention group than the control group (59 (91%) vs 48 (76%)

The mean length of hospital stay was significantly longer in the control group than the intervention group (4.2 vs 1.0 days p <0.001)

Of the patients in the intervention group, 28 had spontaneous passage of stood and 41 had improved abdominal distention.

Results Cont;

Of the 21 patients that required surgical intervention, 6 had segmental bowel resection for bowel ischemia and injury, 15 required LOA. The most common reason for surgery was peritonitis (n=7)

Interpretation

• Adding oral therapy with Mg oxide, L. Acidophilus and Simethicone to standard nonsurgical therapy for partial SBO resulted in a marked reduction in the need for surgical intervention and length of hospital stay compared with nonsurgical treatment alone.

Limitations of Study

• Not double blinded – could lead to potential investigator bias in patient management

• The dx of partial SBO was based clinical presentation and confirmed with the use of plain radiography, but they were not definitively proven with contrast radiography. Therefore, some of the cases successfully treated with the oral therapy may not have been caused by adhesion.

• Study done at only one institution so the validity in generalizing this data is remains unknown.

Thank you!