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|Year : 1977 | Volume
| Issue : 3 | Page : 127-129
Pulmonary edema following lumbar puncture
Department of Tuberculosis and Chest Diseases, L.L.R.M. Medical College, Meerut, 250 102., India
D K Gupta
Department of Tuberculosis and Chest Diseases, L.L.R.M. Medical College, Meerut, 250 102.
Source of Support: None, Conflict of Interest: None
In a boy of 17 years with disseminated tuberculosis, sudden onset of pulmonary edema following lumbar puncture is described. Possible pat ho-mechanisms have been discussed. The link between the lumbar puncture and the development of pulmonary edema is not casual.
|How to cite this article:|
Gupta D K. Pulmonary edema following lumbar puncture. J Postgrad Med 1977;23:127-9
| :: Introduction|| |
Pulmonary edema results when there is an abnormal accumulation of liquid and solute in the extravascular tissues and alveolar spaces of the lung. It may be due to loss of integrity of alveolocapillary barrier or increase in the capillary pressure or decrease in the osmotic pressure leading to an excessive pressure gradient across the alveolo-capillary membrane. Altered premeability of the capillaries or of alveolar epithelium may complicate viral or bacterial infections, inhalation of toxins, ureamia, immunological reactions and defects of coagulation. Increased pulmonary capillary pressure occurs in cardiac disorders such as left ventricular failure, mitral stenosis or myocardial infarction but may also be found in non-cardiac conditions like veno-occlusive disease, pulmonary venous fibrosis, and mediastinal inflammations. Further causes of pulmonary edema include hypoalbuminaemia, lymphatic insufficiency, narcotic overdose, pulmonary embolism, parenchymal lung diseases, cardioversion, cardiopulmonary bypass surgery, high altitude and intravenous fluid therapy because of their effects on the compartments of the lung. Sudden development of pulmonary edema following pleural aspiration ,, and scorpion sting  have also been described.
However, failure to trace in the literature any mention of development of acute pulmonary edema following lumbar puncture has prompted us to report this case.
| :: Case report|| |
A 17 years muslim boy was hospitalized on 12.2.1977 with disseminated tuberculosis of 2 months duration. The illness started with evening rise of temperature, cough with scanty whitish expectoration, night sweats and gradually diminishing appetite. For the last fortnight, fever was continuous. He was having occasional headaches, nausea and vomiting and had grown weaker. At the time of hospitalization he was drowsy, lethargic and with altered consciousness. He also complained of diffuse dull ache in the abdomen but denied any history of alternating diarrhoea and constipation. Previously, he used to get epileptic fits off and on, the last attack being about 3 months prior to admission. No history of injury or diabetes mellitus could be elicited. He was non-vegetarian and used to smoke about 20-30 bidis a day for the last 6 years.
He was ill looking with a pulse rate of 108/ minute, respiratory rate of 22/minute and temperature 38.8° C. Blood pressure was 98/82 mm Hg. He was anaemic. A few minute discrete glands were palpable in the cervical region.
On examination of the chest, a few fine crepitations in the right suprascapular area were found. Examination of the abdomen revealed a soft and tender liver palpable 4.5 cm below right subcostal margin. Diffuse tenderness of the abdomen was present on deep pressure but there was no palpable mass. Neck rigidity and Kernig's sign were positive without any other neurologic deficit. Presence of choroid tubercle could not be demonstrated.
Repeated examination of sputum was found negative for A.F.B. by direct microscopy. Tuberculin test with 1 TU PPD RT 23 Tween 80 gave a sensitivity of 6 mm (negative). Posteroanterior roentgenogram chest (12.2.77) showed miliary shadows throughout both the lung fields. Diagnostic lumbar puncture was done with the following observations: intracranial tension was raised (60 drops/minute), cerebrospinal fluid (CSF) was clear and formed cob-web, protien100 mg%, sugar-42 mg%, chloride-550 mg% and cells-24/mm 3 mainly lymphocytes. Other investigations are shown in [Table 1].
The patient was put on a drug regimen consisting of Inj. Streptomycin sulphate 1 gm I.M. every 12 hours plus Isoniazid 600 mg once a day plus Ethambutol 800 mg once a day along with parenteral corticosteroid every 8 hourly, intravenous mannitol, anti-emetics and vitamin B.. During 11 days of hospitalization 4 bottles of mannitol were administered intermittently and 5 lumbar punctures were performed with a total withdrawal of 24.5 ml CSF. Dexamethasone 4 nig in 2 ml aquous solution was injected intrathecally after 3rd, 4th and 5th procedures. There was some clinical improvement initially but by and large his general condition remained unchanged. CSF protein was continuously rising. On 22.2.77, within an hour of lumbar puncture his general condition suddenly worsened. Pulse rate went upto 136/minute, respiration rate 40/minute and B.P. 80 mm Hg (systolic). He was cyanosed. Both the lung fields were full of bubbling rales which were audible even with nacked ears. Some thin, frothy sputum was dribbling out of his mouth. Measures for pulmonary edema including intratracheal suction of the secretions were instituted immediately, but after a battle of about 5 hours the patient died without any decrease in pulmonary edema. His relatives refused postmortem examination.
| :: Discussion|| |
Pulmonary edema following head injuries, cerebral haemorrhage and certain other neurological conditions in which intracranial pressure is increased, have been reported. ,, Epileptic seizures , and generalised convulsions  may also lead to pulmonary edema. It has been demonstrated that following acute rise in intracranial pressure, significant hemodynamic alterations take place namely rise of systemic, pulmonary arterial and left atrial pressures. ,
In the present case, pulmonary edema developed within an hour of withdrawal of 8 ml CSF (10 ml withdrawal minus 2 ml intrathecal injection of dexamethasone). During his hospital stay of 11 days, only 4 bottles of I.V. mannitol were administered which could not have resulted in overloading of circulation Systemic blood pressures never indicated evidence of hypertension. It is possible that withdrawal of CSF had resulted in `Coning' with cardio-respiratory distress, further acute increase in intracranial pressure and ultimately pulmonary edema. Another possibility is that intracranial hypotension resulting from withdrawal of CSF had brought up hemodynamic alterations in pulmonary circulation through some neurogenic mechanism and sympathetic hyperexcitation. This ultimately had resulted in extravasation of blood elements into the alveoli. However, pathogenesis of pulmonary edema in different conditions appear very complex and no single factor could be held responsible for its sudden appearance.
| :: References|| |
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