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This is only safe under the following conditions:

a) echocardiography has confirmed a moderate to large pericardial effusion;

b) the operator is experienced.

Therapeutic pericardiocentesis is necessary if there is cardiac tamponade (acute life-threatening cardiac impairment).

In populations with high TB/HIV prevalence,TB is the most likely treatable cause of pericardial effusion. It may be safer for the patient to start presumptive anti-TB treatment than to undergo diagnostic pericardiocentesis.

Treatment with steroids and anti-TB drugs, without pericardiocentesis, usually results in satisfactory resolution of tuberculous pericardial effusion.


A possible complication despite TB cure is the development of pericardial constriction. Medical management of heart failure due to pericardial constriction helps in some cases. A surgeon may weigh up the possible benefit to the patient of pericardiectomy, set against the operative risks.

Differential diagnosis

Apart from TB, the differential diagnosis of pericardial effusion includes the following:

transudates: uraemia, heart failure, liver failure, hypothyroidism;

exudates: malignancy, bacterial pericardial empyema, inflammatory diseases.

Tuberculous ascites

Ascites results from peritoneal TB. Routes of spread of TB to the peritoneum include the following:

a) from tuberculous mesenteric lymph nodes;

b) from intestinal TB (pulmonary TB patients may develop intestinal ulcers and fistulae as a result of swallowing infected sputum);

c) bloodborne.

Clinical features

Patients present with constitutional features and ascites. Marked wasting is common in children. Signs of other causes of ascites such as nephrotic syndrome (peripheral and periorbital oedema) or portal hypertension (marked splenomegaly) are usually absent. There may be palpable abdominal masses (mesenteric lymph nodes). Adhesion of nodes to bowel may cause bowel obstruction. Fistulae may develop between bowel, bladder and abdominal wall.


Do a CXR to look for associated PTB.Always do a diagnostic ascitic tap. The aspirated fluid is usually straw-coloured, but occasionally turbid or blood-stained.The fluid is an exudate, usually with more than 300 white cells per mm3 and predominantly lymphocytes. Ultrasound, if available, may show features consistent with TB, including enlarged mesenteric or retroperitoneal lymph nodes.


An ill, wasted patient with TB ascites may have a low serum albumin concentration. In this case, the usual threshold of 30 g/l albumin concentration for diagnosing an exudate is too high. Instead, calculate the difference between the albumin concentrations in serum and ascites. A serum-ascites albumin difference of less than 11 g/l means that the ascites is an exudate.


The diagnosis is usually presumptive. Definitive diagnosis rests on a peritoneal biopsy, available in some hospitals. Blind percutaneous needle biopsy of the peritoneum has a low pick-up rate and a high complication rate. In experienced hands, laparoscopy under local anaesthetic has a high pick-up rate. Laparoscopy enables direct visualization and biopsy of peritoneal TB lesions. Laparotomy will confirm the diagnosis in nearly every case but is too invasive for routine use.

Differential diagnosis

Apart from TB,the differential diagnosis of ascites includes the following:

transudates: heart failure, renal failure, nephrotic syndrome, chronic liver disease due to cirrhosis, hepatosplenic schistosomiasis, hypoproteinaemia;

exudates: malignancy, other infections causing peritonitis. 5.5 TUBERCULOUS MENINGITIS

Routes of spread of TB to the meninges include the following:

a) from rupture of a cerebral tuberculoma into the subarachnoid space;

b) bloodborne.

Clinical features

The patient may present with constitutional features and chronic meningitis. There is gradual onset and progression of headache and decreased consciousness. Examination often reveals neck stiffness and a positive Kernig's sign. Cranial nerve palsies result from exudate around the base of the brain. Tuberculomas and vascular occlusion may cause focal neurological deficits and seizures. Obstructive hydrocephalus may develop. Spinal meningeal involvement causes paraplegia (spastic or flaccid).


The diagnosis usually rests on clinical grounds and cerebrospinal fluid (CSF) examination. In most cases of clinically suspected TB meningitis, lumbar puncture is safe.


Lumbar puncture is hazardous if the patient has a focal neurological deficit (cerebral space-occupying lesion) or if fundoscopy shows papilloedema (raised intracranial pressure). In these circumstances, a CT brain scan is helpful, if available. Otherwise, it may be safer to start presumptive treatment with anti-TB drugs rather than risk lumbar puncture.

The CSF opening pressure is high. The CSF may look clear or occasionally cloudy.The white cell count is usually less than 500 per mm3 with predominantly lymphocytes (or early in the course of infection, predominantly polymorphs). Usually the protein level is high and the glucose low. CSF microscopy shows AFBs in a minority of cases. It is possible to increase the diagnostic pick-up rate by the following:

a) examine the deposit on centrifugation of a 10 ml CSF sample;

b) examine the deposit for at least half an hour before reporting it as negative;

c) examine several CSF samples obtained over a few days.

Lumbar puncture is important for differentiating purulent from TB meningitis. Always exclude cryptococcal meningitis by CSF microscopy (India ink stain) and, if available, fungal culture.

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