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Table of Contents
CASE REPORT
Year : 2014  |  Volume : 30  |  Issue : 4  |  Page : 555-557

Intra-operative post-induction hyperthermia, possibly malignant hyperthermia: Anesthetic implications, challenges and management


1 Department of Anaesthesiology and Critical Care, Batra Hospital and Medical Research Centre, New Delhi, India
2 Department of Pharmacology, M. R. Medical College, Gulbarga, Karnataka, India

Date of Web Publication14-Oct-2014

Correspondence Address:
Michell Gulabani
C-35 Malviya Nagar, New Delhi - 110 017
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0970-9185.142860

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  Abstract 

Malignant Hyperthermia is a pharmacogenetic disorder. Classical manifestations comprise of tachycardia, increase in expired carbon dioxide levels, muscle rigidity, hyperthermia (>38.8°C) and unexpected acidosis. Here we report a case of 16-year-old female patient, ASA-I with chronic rhino-sinusitis and slight strabismus of the left eye posted for functional endoscopic sinus surgery, developing a rise in ETCO 2 and temperature immediately following anesthesia induction. She was aggressively managed to an uneventful recovery. We present a case of intra-operative post-induction hyperthermia possibly MH, its anesthetic implications, challenges encountered and its management.

Keywords: Core temperature monitoring, end tidal carbon dioxide, isoflurane, malignant hyperthermia, propofol


How to cite this article:
Gulabani M, Gurha P, Ahmad S, Dass P. Intra-operative post-induction hyperthermia, possibly malignant hyperthermia: Anesthetic implications, challenges and management . J Anaesthesiol Clin Pharmacol 2014;30:555-7

How to cite this URL:
Gulabani M, Gurha P, Ahmad S, Dass P. Intra-operative post-induction hyperthermia, possibly malignant hyperthermia: Anesthetic implications, challenges and management . J Anaesthesiol Clin Pharmacol [serial online] 2014 [cited 2019 Nov 22];30:555-7. Available from: http://www.joacp.org/text.asp?2014/30/4/555/142860


  Introduction Top


Malignant hyperthermia (MH) is a pharmacogenetic disorder that manifests as potentially fatal hyper-metabolic crisis triggered by volatile anesthetic agents especially halothane and depolarizing muscle relaxants like succinylcholine. Volatile anesthetics activate abnormal RyR-1 receptors resulting in uncontrolled intracellular Ca 2+ release, muscle contraction and metabolic activity. It is a relatively rare disorder showing preponderance among children and adolescents.

MH can either manifest itself in the life-threatening fulminant form or more frequently as a hyperthermic subtle form. Classical manifestations of MH comprise of development of tachycardia, increase in expired carbon dioxide levels, muscle rigidity, increase in body temperature (>38.8°C) and unexpected metabolic and respiratory acidosis. [1]


  Case Report Top


This was a case of a 16-year-old female patient, with non-relevant family history, ASA-I with chronic rhino-sinusitis posted for functional endoscopic sinus surgery. At the pre-anesthetic clinic, the patient presented with a complaint of nasal blockade for 3 months without any fever.

General examination conducted by the anesthetist on duty showed strabismus of the left eye, rest other systemic examination was within the normal limits. No prior exposure to anesthesia was recorded. The patient gave a negative history of any drug use besides those employed for treatment of sinusitis. The body weight recorded was 50 kg and height corresponded to 155 cm and the body mass index was calculated to be 20.8 kg/m 2 . Blood investigations revealed hemoglobin of 10.4, total leucocyte count of 11,000 and platelets of 156,000. Random blood sugar was 86 mg/dl. Vital parameters as noted in the ward chart on the day of surgery were within the normal limits and a temperature of 36.8°C (axillary) was mentioned.

The patient was taken to the operating room, routine monitors in the form of non-invasive blood pressure (BP), SpO 2 probe and three-lead electrocardiogram were applied. Vital parameters prior to induction were within normal limits.

Anesthesia was induced with intravenous midazolam 1 mg, fentanyl 100 μg, propofol 100 mg and vecuronium bromide 5 mg. Patient was mask ventilated by a mechanical ventilator to achieve normocarbia with O 2 and N 2 O and isoflurane (0.9-1 MAC) for approximately 3 min. The trachea was then intubated using endotracheal tube no. 7 mm internal diameter. After confirming endotracheal placement, patient was mechanically ventilated with a tidal volume of 400 ml, respiratory rate 12/min maintaining ETCO 2 32-35 mmHg and an esophageal temperature probe was inserted. The patient was maintained on O 2 , N 2 O and isoflurane (MAC 1).

Immediately following intubation, the ETCO 2 rose up to 60 mmHg, heart rate 120/min, BP 130/90 mmHg, SpO 2 100% and a temperature of 37.8°C were noted. The temperature within a few seconds rose to 38.2°C and within a minute it reached 38.9°C. Isoflurane was stopped and 100% oxygen administered. The surgery was halted and additional assistance was sought from the senior anesthetists in the operating theatre complex.

Intravenous paracetamol infusion and cold sponging were started simultaneously. The ventilator settings were also readjusted to facilitate normocarbia. The ETCO 2 came down to 53 mmHg gradually, but the temperature still continued around 38.9°C. An arterial blood gas (ABG) sample was withdrawn, which showed respiratory acidosis with a pH of 7.30, pCO 2 of 52 mmHg, bicarbonates of 24 mEq and pO 2 of 100 mmHg and K + of 5 mEq/L. Supportive management was aggressively continued and vital parameters were monitored continuously. The patient was intermittently given intravenous midazolam 1 mg and fentanyl 50 μg as bolus twice and N 2 O was continued to prevent awareness.

After 50 min, the temperature came down to 38.6°C and the ETCO 2 normalized completely. In the next 20 min, there was a steady decline in the body temperature and it was recorded to be 38.2°C. The surgery was recommenced by employing intravenous propofol as an infusion in a manually controlled infusion pump while maintaining the patient on O 2 and N 2 O along with intermittent boluses of intravenous fentanyl and vecuronium. The temperature showed a steady pattern of decline to 38°C and then to 37.8°C towards the end of the surgery. An ABG sample was re-sent which depicted a corrected pH of 7.35, pCO 2 of 42 mmHg, bicarbonates of 22 mEq and pO 2 of 100 mmHg.

At the end of the surgical procedure, the anesthesia was reversed and the patient was kept for further observation in the operating room for 15 min. The reversal was overall uneventful and the patient was shifted to the post anesthesia care unit where the vital parameters were found to be within normal limits and the axillary temperature was 37.7°C.


  Discussion Top


MH is an autosomal dominant disorder characterized by genetic heterogeneity. It was brought to the attention of anesthetists just over 50 years ago when Denborough and Lovell described 10 deaths attributable to general anesthetics in a family living in Melbourne, Australia, although the family was thought to originate from Wales. [2]

MH has been thought to be a disease of the western world with just a few cases being reported from the Indian subcontinent. The first detailed case-report of MH from India was published by Saxena and Dua in 2007. [3]

Several predisposing clinical myopathies such as strabismus, ptosis, myotonic dystrophy, muscular dystrophy and Marfan's syndrome have been associated with it. [4] It is associated with mutations in the ryanodine receptor (RyR-1) and physically associated with L-type Ca 2+ channels that function as voltage sensors. The mechanism by which anesthetic agents and depolarizing muscle relaxants trigger MH is not fully understood, but it cannot be ignored that they are etiologic agents and that an early diagnosis is critical for successful treatment. [5]

Isoflurane, a halogenated inhalational anesthetic agent, usually causes an increased amount of cutaneous heat loss thus reducing body temperature marginally, [6] however in susceptible individuals it is invariably linked to MH. [7] MH usually occurs in children and young adults (the incidence of acute MH is highest in the first three decades of life). In most patients, metabolic stimulation is evident clinically within 10 min of administration of volatile anesthetics, whereas in others, several hours may elapse. Hypermetabolism leads to increased carbon dioxide production with associated respiratory acidosis which stimulates the sympathetic nervous system leading to tachycardia. [8]

In a study by Larach et al. [9] gave a clinical grading scale using the clinical indicators for determining the MH raw score. This score has been considered to be a definitive diagnostic indicator of MH based on the clinical findings and biochemical tests. This scale ranks the qualitative likelihood that an adverse anesthetic event represents MH (MH event rank) and that, with further investigation of family history, an individual patient will be diagnosed as MH susceptible (MH susceptibility rank). The scale incorporates six clinical criteria: Evidence of muscle rigidity, muscle breakdown, respiratory acidosis, temperature increase, cardiac involvement and family history. The various parameters have been tabulated in [Table 1] and [Table 2] respectively. Its use may improve MH research by allowing comparisons among well-defined groups of patients.
Table 1: Intra-operative MH diagnostic criteria

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Table 2: MH probability scale

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According to the MH-Raw Score, our patient scored 43 which corresponded to rank 5, i.e., very likely chance of MH. Among the laboratory tests, the caffeine - halothane contracture test (CHCT) is the only generally recognized test for the laboratory diagnosis of MH. Centers world-wide use one of two protocols - either the European MH group protocol [10] or the standards published by the North American MH group. [11]

However, contracture studies are not currently performed in our institution and therefore a standardized CHCT was not possible. Furthermore, studies conducted by Isaacs and Badenhorst [12] point out negative CHCT findings for patients who had full blown MH, thus re-emphasizing the importance of clinical indicators such as the MH-raw score.

Increased carbon dioxide production occurs early, emphasizing the value of continuous capnography. Temperature rise may be a late sign, but core temperature may increase as early as 15 min after exposure to a triggering agent. [13]

The essential points in treatment are the immediate discontinuation of trigger agents, hyperventilation, administration of dantrolene in doses of 2.5 mg/kg, repeated as needed to control signs of MH and cooling by all routes available (especially nasogastric lavage, standard treatment of hyperkalemia). Following a MH episode the patient should be treated with dantrolene for at least 36 h.

Prevention of MH and avoidance of medicolegal action consists of obtaining a thorough history related to anesthetic complications, avoiding MH trigger agents in susceptibles and their relatives, having dantrolene immediately available and monitoring body temperature during general anesthesia. [14]

The major anesthetic challenges faced in a case of MH include hyperthermia, hypercarbia, hyperkalemia and rhabdomyolysis. The anesthetic management of MH must comprise of early identification and removal of possible trigger mechanisms, maintaining normothermia and normocarbia. Dantrolene forms the mainstay of treatment along with supportive management.

 
  References Top

1.
Rosenberg H. Clinical presentation of malignant hyperthermia. Br J Anaesth 1988;60:268-73.  Back to cited text no. 1
[PUBMED]    
2.
Denborough MA, Lovell RR. Anaesthetic deaths in a family. Lancet 1960;276:45.  Back to cited text no. 2
    
3.
Saxena KN, Dua CK. Malignant hyperthermia - A case report. Indian J Anaesth 2007;51:534-5.  Back to cited text no. 3
  Medknow Journal  
4.
White PF, Trevor AJ. Drugs that act in the central nervous system. In: Katzung BG, editor. Basic and Clinical Pharmacology. 11 th ed. New York: McGraw-Hill Medical Publishing Division; 2009. p. 423-37.  Back to cited text no. 4
    
5.
Zhou J, Allen PD, Pessah IN, Mohamed N. Neuromuscular disorders and malignant hyperthermia. In: Miller RD, editor. Miller's Anesthesia. 7 th ed. New York: Church Hill Livingstone Elsevier; 2009. p. 2538-40.  Back to cited text no. 5
    
6.
Sessler DI, McGuire J, Moayeri A, Hynson J. Isoflurane-induced vasodilation minimally increases cutaneous heat loss. Anesthesiology 1991;74:226-32.  Back to cited text no. 6
    
7.
Joseph MM, Shah K, Viljoen JF. Malignant hyperthermia associated with isoflurane anesthesia. Anesth Analg 1982;61:711-2.  Back to cited text no. 7
    
8.
Hines RL, Marschall KE. Pediatric diseases. In: Hines RL, Marschall KE, editors. Stoelting's Anesthesia and Co-Existing Disease. 5 th ed. Philadelphia: Saunders; 2008. p. 701-7.  Back to cited text no. 8
    
9.
Larach MG, Localio AR, Allen GC, Denborough MA, Ellis FR, Gronert GA, et al. A clinical grading scale to predict malignant hyperthermia susceptibility. Anesthesiology 1994;80:771-9.  Back to cited text no. 9
    
10.
A protocol for the investigation of malignant hyperpyrexia (MH) susceptibility. The European Malignant Hyperpyrexia Group. Br J Anaesth 1984;56:1267-9  Back to cited text no. 10
    
11.
Larach MG. Standardization of the caffeine halothane muscle contracture test. North American Malignant Hyperthermia Group. Anesth Analg 1989;69:511-5.  Back to cited text no. 11
    
12.
Isaacs H, Badenhorst M. False-negative results with muscle caffeine halothane contracture testing for malignant hyperthermia. Anesthesiology 1993;79:5-9.  Back to cited text no. 12
    
13.
Hopkins PM. Malignant hyperthermia: Advances in clinical management and diagnosis. Br J Anaesth 2000;85:118-28.  Back to cited text no. 13
    
14.
Rosenberg H, Brandom BW, Sambuughin N, Fletcher JE. Malignant hyperthermia and other pharmacogenetic disorders. In: Barash PG, editor. Barash Clinical Anesthesia. 5 th ed. New York: Lippincott Williams & Wilkins; 2007. p. 530-40.  Back to cited text no. 14
    



 
 
    Tables

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