대한마취과학회지 2006; 50: S 71∼3 Korean J Anesthesiol Vol. 50, No. 6, June, 2006
□ 영문논문 □
Cardiac Arrest due to Severe Hypokalemia during Barbiturate Coma Therapy in a Patient with Severe Acute Head Injury -A case reportDepartments of 1Anesthesiology and Pain Medicine, 2Neurosurgery, 3Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju, Korea
Il-Woo Shin, M.D.1, Ju-Tae Sohn, M.D.1,3, Ju-Young Choi, M.D.1, Heon Keun Lee, M.D.1, Chul-Hee Lee, M.D.2, and Young-Kyun Chung, M.D.1
An emergency left frontotemporal craniectomy with direct neck clipping and hematoma removal was performed in a 36-year-old man with a ruptured left middle cerebral artery aneurysm and sylvian hematoma. Because of severe brain swelling postoperatively, we induced barbiturate coma therapy to treat his intractable brain swelling. He had an initial loading dose of sodium thiopental (5 mg/kg) followed by continuous infusion of sodium thiopental (5 mg/kg/hour). The lowest potassium concentration recorded during the barbiturate coma therapy was 1.1 mmol/L; necessitating treatment with cardiac massage, epinephrine, and atropine because of asystole and severe bradycardia. However, he did not recover from cardiac arrest. We present here a case of cardiac arrest due to severe life threatening hypokalemia that occurred during barbiturate coma therapy. (Korean J Anesthesiol 2006; 50: S 71∼3) ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ Key Words: barbiturate coma, cardiac arrest, hypokalemia.
Barbiturate coma therapy has been used for several years in
at university hospital with a subarachnoid hemorrhage (Hunt
the treatment of patients with severe intractable intracranial
Hess grade IV) and acute sylvian hematoma due to a ruptured
hypertension. The side effects1) encountered during barbiturate
MCA aneurysm visualized on a brain computerized tomogram.
coma therapy include arterial hypotension, electrolyte imbal-
An emergency left frontotemporal craniectomy with direct neck
ance,2,3) respiratory complications, hepatic dysfunction and renal
clipping of the left MCA aneurysm and left sylvian hematoma
dysfunction. Dramatic changes in serum potassium are not
removal was performed on his admission. The intracranial pressure
common in patients with increased intracranial pressure who
(ICP, Brain-Pressure monitor Model: HDM 13.3, Spiegelberg,
receive high-dose barbiturates. We present here a case of
Germany) was monitored postoperatively. He had severe brain
cardiac arrest due to severe life threatening hypokalemia that
swelling that was observed on the brain computerized tomogram
occurred during barbiturate coma therapy in a patient with
taken postoperatively, and ICP increased to 37.9 mmHg post-
direct surgical clipping of a ruptured middle cerebral artery
operatively. Therefore, the patient was moderately hyperventilated (PaCO2: 29-32 mmHg) and mannitol (6 × 37.5 g/day) was
(MCA) aneurysm and sylvian hematoma removal.
used to control the ICP. We then started barbiturate coma therapy to treat the intractable brain swelling 7 hours after the
CASE REPORT
operation. He had an initial loading dose of sodium thiopental A 36-year-old man was admitted to the intensive care unit
(5 mg/kg) followed by a continuous infusion of sodium thiopental (5 mg/kg/hour) (Fig. 1). His EEG displayed burst suppression during barbiturate coma therapy. The ICP was
Received : December 29, 2005 Corresponding to : Ju-Tae Sohn, Gyeongsang National University College of Medicine, 90 Chilam-dong, Jinju 660-702, Korea. Tel: 82-55-7508141, Fax: 82-55-750-8142, E-mail:
[email protected] Presented in the annual meeting of the American Society of Anesthesiologists, Atlanta, Georgia, October 25, 2005.
controlled after barbiturate coma therapy was started, and the ICP was decreased to 10.5 mm Hg. He received intravenous dopamine
(5-20μg/kg/min)
and
dobutamine
(5-20μg/kg/min)
4 hour after barbiturate coma therapy was started to maintain S 71
Korean J Anesthesiol：Vol. 50. No. 6, 2006
Fig. 1. Changes of intracranial pres+ sure (ICP), serum potassium (K ) levels, and arterial blood pH with respect to potassium supplementation and thiopental infusion before (A: emergency room), during (B: operation) and after the operation.
blood pressure. He received a total of 55 mmol of potassium
during barbiturate coma therapy probably did not cause
over the postoperative period of 16 hours. The lowest serum
hypokalemia (potassium; 2.8 mmol/L), because dopamine in-
potassium
coma
fusion was started 4 hours after the barbiturate coma therapy
therapy was 1.1 mmol/L (Fig. 1), which necessitated drastic
was started. Induced hypothermia (32oC) has been used as a
intervention with cardiac massage, epinephrine (1 mg), and
potential treatment for neurologic trauma, and is associated
atropine (0.5 mg). We then had to discontinue the barbiturate
with severe electrolyte disturbances, such as hypokalemia,
infusion because of asystole and severe bradycardia. The severe
hypomagnesemia, and hypophosphatemia.7) As this patient was
hypokalemia induced cardiac arrest, and cardiopulmonary resus-
at stable normothermia during the barbiturate coma therapy,
citation was unsuccessful. His body temperature was stable
hypothermia-induced polyuria7) did not induce the hypokalemia
normothermia throughout treatment. The arterial blood pH was
observed in this case. For patients with severe head trauma
normal (pH 7.35) or moderately acidotic (pH 7.15) before and
and the potential risk of excessive catecholamine release,
during the barbiturate coma therapy, respectively (Fig. 1).
special attention must be given to excessive hypokalemia and
concentration
recorded
during
barbiturate
hyperkalemia following head injury.8) An intracellular potassium shift due to increased plasma catecholamine8,9) (norepinephrine,
DISCUSSION
epinephrine)-induced beta-2-adrenergic stimulation of the sodiumHigh-dose barbiturate coma therapy has been used for
potassium pump may have been partially involved in this
hemodynamically stable and salvageable severe head injury
hypokalemia.
patients that suffer from intracranial hypertension that is re-
This patient received 1,000 cc of 15% mannitol before
fractory to the maximal medical and surgical intracranial
barbiturate coma therapy. However, a previous study10) reported
pressure-lowering therapy.4) The immediate complications from
that intravenous 20% mannitol (1.4 g/kg) administration does not
high-dose barbiturate therapy include tachycardia and hypoten-
induce hypokalemia in a patient with a brain tumor. Some re-
sion.5) The delayed complications from high-dose barbiturate
ports11,12) indicate that an increase in plasma osmolality induced
therapy include hypokalemia, liver dysfunction, infection, cardiac
by administration of mannitol causes an increase in plasma potas-
failure and renal failure.5)
sium due to the shift of potassium from cells to the extracellular
Several factors, including catecholamine levels, body temperature,
fluid. In addition, serum potassium increased from 3.7 mmol/L
acid-base balance, severe acute head injury, barbiturates, and
to 4.6 mmol/L (Fig. 1) before barbiturate coma therapy. Taking
mannitol, can affect serum potassium levels, as was seen in
into consideration the above facts and reports,10-12) it seems
this case. Dopamine infusion (10, 30μg/kg/min) induces hypo-
highly unlikely that polyuria due to mannitol administration alone
kalemia in dogs through beta-2-adrenergic stimulation of the
caused this kind of severe hypokalemia.
sodium-potassium pump.6) However, the infusion of dopamine
Induction of barbiturate coma is accompanied by a physiS 72
Il Woo Shin, et al : Hypokalemia and Barbiturate Coma
2. Cairns CJS, Thomas B, Fletcher S, Parr MJA, Finfer SR: Life-threatening hyperkalemia following therapeutic barbiturate coma. Intensive Care Med 2002; 28: 1357-60. 3. Ok SH, Chung YW, Sohn JT, Jung JM, Chung YK: Severe hypokalemia occurring during barbiturate coma therapy in a patient with severe acute head injury. Acta Anaesthesiol Scand 2005; 49: 883-4. 4. The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care: Use of barbiturates in control of intracranial hypertension. J Neurotrauma 2000; 17: 527-30. 5. Oda S, Shimoda M, Yamada S, Sato O, Tsugane R: Problems in general management during barbiturate therapy. No Shinkei Geka 1992; 20: 1241-6. 6. Drake HF, Smith M, Corfield DR, Treasure T: Continuous multi-channel intravascular monitoring of the effects of dopa- mine and dobutamine on plasma potassium in dogs. Intensive Care Med 1989; 15: 446-51. 7. Polderman KH, Peerdeman SM, Girbes ARJ: Hypophosphatemia and hypomagnesemia induced by cooling in patients with severe head injury. J Neurosurg 2001; 94: 697-705. 8. Schaefer M, Link J, Hannemann L, Rudolph KH: Excessive hypokalemia and hyperkalemia following head injury. Intensive Care Med 1995; 21: 235-7. 9. Pomeranz S, Constantini S, Rappaport ZH: Hypokalemia in severe head trauma. Acta Neurochir 1989; 97: 62-6. 10. Schettini A, Stahurski B, Young HF: Osmotic and osmotic-loop diuresis in brain surgery effects on plasma and CSF electrolytes and ion excretion. J Neurosurg 1982; 56: 679-84. 11. Seto A, Murakami M, Fukuyama H, Niijima K, Aoyama K, Takenaka I, et al: Ventricular tachycardia caused by hyperkalemia after administration of hypertonic mannitol. Anesthesiology 2000; 93: 1359-61. 12. Hirota K, Hara T, Hosoi S, Sasaki Y, Hara Y, Adachi T: Two cases of hyperkalemia after administration of hypertonic mannitol during craniotomy. J Anesth 2005; 19: 75-7. 13. Nordstrom CH, Messeter K, Sundbarg G, Schalen W, Werner M, Ryding E: Cerebral blood flow, vasoreactivity, and oxygen consumption during barbiturate therapy in severe traumatic brain lesions. J Neurosurg 1988; 63: 424-31. 14. Rehncrona S, Rosen I, Siesjo BK: Brain lactic acidosis and ischemic cell damage: 1 biochemistry and neruophysiology. J Cereb Blood Flow Metab 1981; 1: 297-311. 15. Nilsson L, Siesjo BK: The effect of anesthetics on the tissue lactate, pyruvate, phosphocreatine, APT and AMP concentrations, and on intracellular pH in the rat brain. Acta Physiol Scand 1970; 80: 142-4. 16. Messeter K, Ponten U, Siesjo BK: The influence of deep barbiturate anesthesia upon the regulation of extra- and intra cellular pH in the rat brain during hypercapnia. Acta Physiol Scand 1972; 85: 174-82. 17. Hall RJC, Cameron IR: The effect of pentobarbitone on plasma and intracellular sodium, potassium and pH in rabbit cardiac and skeletal muscle. Clin Sci 1979; 57: 549-51. 18. Bali IM, Dundee JW, Assaf RAE: Immediate changes in plasma potassium induced by intravenous induction agents. Br J Anaesth 1974; 46: 929-33.
ological decrease in cerebral blood flow and the calculated cerebral metabolic rate of oxygen; leading to a rapid and lasting decrease in ICP.13) The high degree of tissue lactic acidosis during brain ischemia can impair postischemic recovery.14) Barbiturates are associated with a decrease in lactate production and the lactate/pyruvate ratio; as well as with increased intracellular pH in the rat brain.15) Compared with a control state, the reduction of cerebral energy metabolism during barbiturate treatment increases intracellular pH in the rat brain by 0.04-0.09 units during normocapnia.16) When taking into consideration the above reports,14-16) it is probable that the protective effects of barbiturate coma therapy are associated with increased pH through the decreased lactate production that produces the intracellular potassium shift. Pentobarbitone anaesthesia causes hypokalemia because of the movement of potassium between the extracellular and intracellular compartments in rabbit cardiac and skeletal muscle.17) Induction of barbiturate anesthesia causes a transient and significant hypo- kalemia in humans.18) Before barbiturate coma therapy was started, serum potassium increased from 3.7 mmol/L to 4.6 mmol/L. However, after barbiturate coma therapy was started, serum potassium decreased from 4.6 mmol/L to 2.8 mmol/L with a concomitant decrease of ICP to 10.5 mmHg (Fig. 1). Taking into consideration the above studies14-18) and facts, we propose that a shift of potassium from the extracellular to intracellular space caused the severe hypokalemia. Plasma potassium levels and potassium balance (total potassium infusion minus urinary potassium loss) must be closely monitored for all patients with severe acute brain injury during barbiturate coma therapy. If the severe hypokalemia will be encountered during barbiturate coma, we think that it is reasonable to seek other methods to reduce the increased ICP. Further study is needed to elucidate a detailed mechanism associated with the severe changes in plasma potassium levels that occur both during and after barbiturate coma therapy in patients with severe acute brain injury. This case serves to illustrate that the clinician must be aware of the potential occurrence of severe hypokalemia, which may be occasionally encountered during barbiturate coma therapy in a patient with severe acute head injury.
REFERENCES 1. Schalen W, Messeter K, Nordstrom CH: Complications and side effects during thiopentone therapy in patients with severe head injuries. Acta Anaesthesiol Scand 1992; 36: 367-77.
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