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CASE REPORT
Year : 2009  |  Volume : 53  |  Issue : 4  |  Page : 486-488 Table of Contents     

Ketamine and Pulmonary Oedema-Report of Two Cases


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 Publication3-Mar-2010

Correspondence Address:
S Parthasarathy
Govt. Dist. Hgrs Hospital, Kumbakonam
India
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Source of Support: None, Conflict of Interest: None


PMID: 20640214

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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 Top


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 Top


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 Top


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.



 
   References Top

1.Schwin DA. Cardiac pharmacology: Cardia anaesthesia principles and practice; second edition, Fawry G,Paul G Barasch,Reve JG (eds) Lippincott willkins and Will­iams Philadelphia 2001;73-82.  Back to cited text no. 1      
2.Levy GJ, Shabot MM, Hart ME, Mya WW, Goldfinger D. Transfusion-associated noncardiogenic pulmonary edema. Report of a case and a warning regarding treat­ment Transfusion 2003;26: 278-281.  Back to cited text no. 2      
3.Tom a G Amcheslavsky\ Zelman\ DeWittD,ProughD. Neurogenic pulm onary edema: Pathogenesis, clinical pic­ture, and clinical management. Seminars in Anesthesia. Perioperative Medicine andPain 2004;23: 221-229.  Back to cited text no. 3      
4.Gardaz JP, ForsterA, Suter PM . Non-cardiac acute ful­minating pulmonary edema occurring at the end of an­esthesia . Can Anaesth Soc J 1979;26:34-7.  Back to cited text no. 4      
5.StoeltingRK. Pharm acologyand PhysiologyinAnesthetic Practice, 2nded. Philadelphia: JB LippincottCo.,1991.  Back to cited text no. 5      
6.6.. William BermanJr,Raymond R.Fripp,Mark Rublerand Lorraine Alderete. Hemodynamic effects of ketamine in children undergoing cardiac catheterization. Pediatric Cardiology 1990;11:72-76.  Back to cited text no. 6      
7.Singh PP, Dim ich I, Shamsi A. Intraoperative pulmonary oedema in ayoung cocaine smoker. Can JAnaesth 1994; 41:961-4.  Back to cited text no. 7      
8.Lang SA, Duncan PG, Shephard DAE, Ha HC. Pulmo­nary oedema associated with airway obstruction. Can J Anaesth 1990; 37: 210-8.  Back to cited text no. 8      
9.Tamow J,Hess W Pulmonary hypertension and edema after intravenous ketamine. Anaesthesist 1978;27:486­7.  Back to cited text no. 9      
10.Pandey CK, Mathur N, Singh N, et al. Fulm inapt pulmo­nary edema after intramuscular ketamine. Canadian Jour­nal ofAnaesthesia 2000;47:894-6.  Back to cited text no. 10      
11.Murphy IL Jr. Hypertension and pulmonary oedema as­sociated with ketam me administration in a patient with a history of substance abuse. Can J Anaesth 1993; 40: 160-1.  Back to cited text no. 11      
12.Tegmann GF. Hypoxemia and suspected pulmonary oedem a in a Dorper ewe after diazepam-ketamine induc­tion of anaesthesia. J S Mr Vet Assoc 2000;71:64-5.  Back to cited text no. 12      




 

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