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| CASE REPORT |
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| Year : 2009 | Volume
: 53
| Issue : 4 | Page : 486-488 |
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Ketamine and Pulmonary Oedema-Report of Two Cases
S Parthasarathy1, M Ravishankar2, S Selvarajan3, T Anbalagan4
1 Chief Anaesthesiology, Govt. Dist. Hg Hospital, Kumbakonam, India
2 Professor, Mahatma Gandhi Medical College and Research Institute, Pondicherry, India
3 Consultant Surgeon, Govt. Dist. Hg Hospital, Kumbakonam, India
4 ConsultantAnaesthesiologists, Govt. Dist. Hg Hospital, Kumbakonam, India
| Date of Web Publication | 3-Mar-2010 |
Correspondence Address:
S Parthasarathy
Govt. Dist. Hgrs Hospital, Kumbakonam
India
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 20640214 
Perioperative pulmonary oedema is one of the most challenging complications faced by anaesthesiologists. In most of the instances, coronary artery disease, valvular heart diseases, hypertension may precipitate pulmonary oedema due to increased hydrostatic pressure while acid aspiration, airway obstruction may cause it due to increased vascular permeability. In a few instances, acute pulmonary oedema can present in an otherwise healthy patient to cause diagnostic difficulties. We report two such cases of intra operative pulmonary oedema with the use of ketamine which were identified and managed successfully. The most probable cause is also described. Keywords: Pulmonary oedema, Perioperative, Ketamine
How to cite this article:
Parthasarathy S, Ravishankar M, Selvarajan S, Anbalagan T. Ketamine and Pulmonary Oedema-Report of Two Cases. Indian J Anaesth 2009;53:486-8 |
How to cite this URL:
Parthasarathy S, Ravishankar M, Selvarajan S, Anbalagan T. Ketamine and Pulmonary Oedema-Report of Two Cases. Indian J Anaesth [serial online] 2009 [cited 2020 Nov 28];53:486-8. Available from: https://www.ijaweb.org/text.asp?2009/53/4/486/60323 |
 Introduction | |  |
Pulmonary oedema's the abnormal accumulation of fluid in the interstitial or alveolarspaces of the lung. It occurs for a number of reasons which can be explained on the basis of a disturbance in the normal Starling equation. It involves changes in hydrostatic or oncotic pressure across the alveolar membrane or in the permeability of the alveolar membrane such that fluid moves across from the capillaries into the alveolar space [1] . Traditional teaching's thatpulmonary oedema occurring in patients tends to be cardiac in aetiology, with usually left heart dysfunction causing back pressure across the pulmonary system, resulting in extravasation of fluid into the alveoli. In patients undergoing anaesthesia, increased afterload as in neurogenic pulmonary oedema and othernon cardiogenic causes are also encountered [2],[3],[4] . Ketamine is a widely used anaesthetic agentwith proven circulatory changes. We encountered two cases of intraoperative pulmonary oedema with the use of ketamine as the anaesthetic agent which are reported below.
| Case Reports | | |
Case 1. A 27-year-old 60 kg healthy male presented for testicular biopsy. Preoperative investigations including a routine ECG were normal. Atropine 0.5 mg, diazepam 5 mg and ketamine 100 mg were administered intravenously. Noninvasive blood pressure, pulse oximeter and ECG monitoring were applied. He was given 100% O z with a normalregular spontaneous respiration. Pulse rate was 85/min. and blood pressure was maintained at 130/80 mm Hg. Ten minutes later the patient desaturated and SpO 2 came to around 6570%. Respiration was shallow with a rate of around 35/min. There was neither suprastemal nor supraclavicular retraction. There was no rocking horse movement of the chest to prove respiratory obstruction. There was neither active wheeze nor vomitus in the mouth to suggest acid aspiration. The heart rate increased to 130/min. with scattered basal crepitations.The blood pressure was 120/80. As the patient desaturated further, he was intubated immediately. The patient allowed intubation without muscle relaxants and given positive pressureventilation (IPPV). In a short time, the bag was tight with increased resistance to ventilation and soon there was pinkfrothy fluid from the endo tracheal tube. He was managed with intravenous fmsemide 100 mgand IPPV with pressure controlled ventilation continued. With this, the clinical profile improved. The heart rate settled down between 90-100/min. The conscious status progressed and in the next hour, IPPV was discontinued and the patient was maintained with `T' piece with satisfactory respiratory rate of around 20-25/min and stable haemodynamics. The patient was extubated after three hours. Postoperative chest x ray was normal. Our town doesn't have the facility of blood gas analysis. He was discharged in two days in normal condition.
Case 2. Atwo-year-old healthy male child weighing 12 kg presented for circumcision. Routine preoperative investigations were normal. Ketamine 25 mg, atropine 0.2 mg and diazepam 2 mg were administered intravenously. Pulse oxi neher and precordial stethoscope were the monitors applied. Forthe fu stten minutes the baby was nonnalwith SpO 2 of 100% and heart rate of around 100/min. The patient started to desaturate slowly in the next 10 minutes with SpO 2 decreasingto 50%. There was neither clinical airway obstruction nor aspiration. Respiratory rate went upto 45/min with minimal basal crepitations. The clinical scenario worsened to allow intubation. Endotracheal intubation was done and IPPV instituted with a tight bag and frothy pink fluid was coming fromthe tube. Fiusemide 10 mg with dexamethasone 1 mg was given intravenously. IPPV was continued in the PCV mode according to our accepted protocols and settings forthe next two hour. Withthis management, the patient improved significantly with regardto respiratory rate, Sp0 2 and added sounds in the lung. The conscious status came to normal. Later the child was extubated after aTpiecetrial of one hour. The patienthad atotally uneventful postoperative period. Aprobable diagnosis of ketamine induced pulmonary oedemawas made.
| Discussion | | |
Ketamine is an induction agent with distinct analgesia, rapid onset of action with short duration. It is used extensively in developing countries because of its low cost. Ketamine is a potent sympathomimetic agent. In normal patients, it produces increased pulmonary artery pressure, increased pulmonary vascular resistance, and increased right ventricular stroke work. Ketamine causes tachycardia, hypertension and bronchodilation. These effects mimic sympathetic stimulation [5] . Ketamine increases heart rate, cardiac output and pulmonaty arterialpres sure (PAP). The rise in PAP is more consistent than the rise in PVR; resistance changes were greatest in patients with elevated resting PVR [6] . Stimulation of CNS (central nervous system) to increase sympathetic nervous system outflow is one of the proposed mechanism. The other is the inhibition of norepinephrine uptake in the postganglionic sympathetic nerve endings to elevate plasma catecho lamine levels. These may explain the onset of pulmonary edema in cocaine addicts with ketamine [7] . We neither encountered active wheezing nor aspirate in the mouth or orophatynx. Hence in our cases the possibility ofpulmonary oedema either due to respiratory obstruction [8] or aspiration was ruled out on clinical grounds. As there is a distinct analgesia with the use of ketamine and the surgery beingminorwe did not use any added analgesics. Hence the diagnosis was centered on two possible causes of pulmonary oedema.
l. Ketamineitselfproducingpulmonaty oedema either by direct stimulation of CNS to effect a sympathetic discharge or inhibition ofnorepinephrine uptake in the po stganglionic sympathetic nerve endings to elevate plasma catecholamine levels. At least one such case is reported in a patient with coronary artery diseas e [9] and another in ahealthy child for dressing of bums wound [10] . Hypertension and pulmonary oedema are more likely after ketamine in patients with substance abuse [11] and use ofketamine should be cautious and in such patients.
2. Propylene glycol [12] , an organic solvent in the preparation ofdiazepam is reported to cause stimulation of vaso active substances to result in pulmonary oedema. Reports of this solvent producing such complication are reported in animals. Because of its extreme rarity and lack of human reports with propylene glycolwe concluded the probable cause could be due to the use of ketamine.
Ketamine, an anaesthetic agent with unique advantages has got widespread use in clinical practice. We reporttwo cases of pulmonary oedema following ketamine use to caution the casualusers of the drug and to create awareness aboutthis possibility in undiagnosed cases of perioperative pulmonary oedema.
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