Acute Intestinal Pseudo Obstruction

Also known as: Ogilvie syndrome

Acute colonic pseudo obstruction, or Ogilvie syndrome, is acute colonic dilatation without a mechanical obstruction.

It occurs particularly in severely ill, postoperative, trauma, neurological, cardiac and metabolically disturbed patients. Drugs including opioids and anticholinergic agents may precipitate or worsen it.

The caecum is at greatest risk of ischaemia and perforation because wall tension rises as diameter increases.

Check potassium, magnesium, calcium, renal function and markers of systemic illness. Correctable metabolic causes should be actively sought.

CT abdomen and pelvis with IV contrast: confirms colonic dilatation without a mechanical transition point and excludes volvulus or obstructing tumour.

A caecal diameter approaching or exceeding 12 cm, prolonged distension and worsening symptoms increase perforation risk. ASGE defines uncomplicated disease as absence of ischaemia, peritonitis and perforation with caecal diameter below 12 cm.

For uncomplicated disease, initially correct the precipitating factors for up to about 48 to 72 hours:

Keep fasting initially if markedly distended
Correct potassium, magnesium and fluid abnormalities
Stop opioids and anticholinergic drugs where possible
Mobilise and reposition frequently
Treat sepsis, cardiac, respiratory or neurological triggers
Use nasogastric decompression when significant upper gastrointestinal distension or vomiting is present

If significant distension persists despite conservative treatment and there is no contraindication, give:

Neostigmine 2 mg IV over 3 to 5 minutes with continuous cardiac monitoring and immediate availability of atropine because clinically important bradycardia can occur. A second 2 mg dose may be given if the first dose fails and the patient remains an appropriate candidate.

Avoid neostigmine in mechanical obstruction or perforation. Significant bradyarrhythmia and severe active bronchospasm are important contraindications or cautions.

Colonoscopic decompression with placement of a decompression tube is appropriate when neostigmine is contraindicated or unsuccessful.

Peritonitis, perforation or bowel ischaemia requires surgery. Surgical options depend on bowel viability and may include caecostomy or colectomy, but operative mortality is substantial in these often critically ill patients.

Hypersplenism

Hypersplenism is excessive sequestration and destruction of circulating blood cells by an enlarged or hyperfunctioning spleen.

The characteristic clinical pattern is:

Splenomegaly
One or more peripheral cytopenias
Preserved or compensatory bone marrow production

Cytopenia can involve:

Platelets
Red cells
White cells

or all three cell lines.

Thrombocytopenia is often the most prominent abnormality because a normal spleen already sequesters a substantial fraction of circulating platelets.

Hypersplenism is a syndrome caused by another disorder, not a final diagnosis.

Important causes include:

Portal and congestive

Cirrhosis
Portal hypertension
Portal or splenic vein thrombosis

Haematological

Myelofibrosis
Lymphoma
Leukaemia
Haemolytic anaemia
Thalassaemia

Infectious

Malaria
Visceral leishmaniasis
Chronic systemic infection

Inflammatory

Felty syndrome

Storage disease

Gaucher disease

The spleen can become markedly enlarged and hyperfunctional in many of these conditions.

Patients can present with consequences of the enlarged spleen:

Left upper quadrant discomfort
Early satiety
Abdominal fullness
Mechanical pressure symptoms

or consequences of cytopenia:

Thrombocytopenia

Easy bruising
Mucosal bleeding
Prolonged bleeding

Anaemia

Fatigue
Dyspnoea
Tachycardia

Leukopenia or neutropenia

Recurrent bacterial infection

A patient can have substantial hypersplenism without spontaneous bleeding because platelet function and hepatic coagulation status also influence bleeding risk.

Initial evaluation should establish both the presence of cytopenia and the underlying disease.

Obtain:

Full blood count with differential
Peripheral blood film
Reticulocyte count
Liver function
Coagulation profile
Renal function
Haemolysis profile where relevant
Disease specific investigations according to clinical context

Ultrasound or CT defines splenic size and evaluates:

Portal vein
Splenic vein
Liver morphology
Lymphadenopathy
Focal splenic lesion

Bone marrow

Bone marrow examination is not required simply to prove hypersplenism.

It is appropriate when:

Haematological malignancy is possible
Pancytopenia remains unexplained
Marrow failure must be distinguished from peripheral sequestration
Myelofibrosis is suspected

A hypocellular failing marrow argues against uncomplicated hypersplenism as the sole explanation for cytopenia.

Treat the underlying cause

This is the first priority.

Examples include:

Portal hypertension treatment
Antimalarial treatment when infection is confirmed
Disease directed therapy for lymphoma or leukaemia
Myelofibrosis directed systemic therapy
Treatment of autoimmune disease

Do not perform splenectomy merely to normalise an abnormal full blood count when the underlying disease can be treated directly.

Blood product support

Transfuse according to clinical need, not simply to normalise laboratory values.

Platelet transfusion in severe hypersplenism can produce only transient increases because platelets are rapidly sequestered.

Reserve transfusion for:

Clinically significant bleeding
Major invasive procedure
Critical thrombocytopenia with a high bleeding risk

Indications for splenectomy

Consider splenectomy when hypersplenism produces clinically important morbidity despite appropriate treatment of the underlying disorder, such as:

Recurrent clinically significant bleeding from severe thrombocytopenia
Severe symptomatic anaemia or transfusion dependence caused predominantly by splenic sequestration or destruction
Recurrent infection from severe neutropenia
Painful or mechanically disabling splenomegaly
Recurrent splenic infarction
Rupture risk or previous rupture

The expected haematological benefit must be weighed against lifelong:

Infection risk
Thrombosis risk
Operative morbidity

Partial splenic embolisation

Partial splenic artery embolisation can reduce functional splenic mass without complete removal.

It is useful in selected patients who:

Have major portal hypertension
Are poor operative candidates
Need improvement in cytopenia

Complications include:

Severe post embolisation pain
Fever
Splenic infarction
Abscess
Portal vein thrombosis

Excessive embolisation increases major complication risk.

Portal hypertension

Splenectomy may improve hypersplenic thrombocytopenia but does not correct the underlying portal hypertensive physiology.

Patients with cirrhosis and very large spleens have an important postoperative risk of portal and splenic venous thrombosis, so surgery should not be undertaken solely for a mildly low platelet count.

Acute Intestinal Pseudo Obstruction

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management