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(Chest. 2006;129:800-804.)
© 2006 American College of Chest Physicians

Glucose-Insulin and Potassium Infusions in Septic Shock*

Shahir S. Hamdulay, BSc, MRCP; Ali Al- Khafaji, MD, MPH, FCCP and Hugh Montgomery, MD, MRCP

* From the Department of Intensive Care Medicine (Drs. Hamdulay and Montgomery), University College London Foundation Hospitals, The Middlesex Hospital, London, UK; and Department of Intensive Care Medicine (Dr. Al-Khafaji), University of Pittsburgh School of Medicine, Pittsburgh, PA.

Correspondence to: Shahir Hamdulay, BSc, MRCP, Department of Medicine, Hammersmith Hospital, Du Cane Rd, London W12 0HS, UK; e-mail: sh_hamdu{at}hotmail.com


   Abstract
TOP
 Abstract
Introduction
 Case 1
 Case 2
 Discussion
 References
 
Glucose-insulin and potassium (GIK) infusions are beneficial in treating ischemic myocardial depression. Myocardial depression is also an important feature in septic shock. We describe two cases of pressor-resistant hypodynamic septic shock that responded to high-dose GIK infusions. In each case, hemodynamic profiles improved sufficiently to allow withdrawal of vasopressor agents. Further assessment of GIK in patients with hypodynamic septic shock is necessary to confirm efficacy and prognostic significance.

Key Words: antiinflammatory • glucose-insulin and potassium • insulin • myocardium • sepsis • shock


   Introduction
TOP
 Abstract
 Introduction
Case 1
 Case 2
 Discussion
 References
 
Septic shock carries a high attendant risk of death to which impaired myocardial contractility may contribute. Recent interest in the use of glucose-insulin and potassium (GIK) infusions as therapy in ischemic myocardial depression has extended to septic myocardial depression. Few studies have demonstrated an improvement in the hemodynamics of hypodynamic septic shock on commencing GIK infusions. We describe two cases of hypodynamic septic shock in which such intervention was associated with an improvement in hemodynamic profile.


   Case 1
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 Abstract
 Introduction
 Case 1
Case 2
 Discussion
 References
 
A 51-year-old woman with high-grade B-cell lymphoma (stage IIIb) had dyspnea 2 days following a second course of chemotherapy with cyclophosphamide, adriamycin, vincristine, and prednisolone. She was jaundiced, febrile (39°C), tachycardic (120 beats/min), and hypotensive (90/60 mm Hg) with evidence of right middle lobe consolidation. Investigations revealed low arterial oxygen saturation (88% on room air); pancytopenia (hemoglobin, 7 g/dL; WBC, 1.6 x 109/L; neutrophils, 0.8 x 109/L; platelets, 18 x 109/L); coagulopathy (prothrombin time [PT], 18 s; activated thromboplastin time [APTT], 38 s; thrombin time [TT], 12 s); deranged liver function test results (bilirubin, 266 µmol/L; alanine aminotransferase, 542 IU/L; alkaline phosphatase, 90 IU/L; albumin, 17 g/dL); and abnormal biochemistry results (urea, 12.2 mmol/L; creatinine, 112 mmol/L; sodium, 140 mmol/L; potassium, 5.1 mmol/L; C-reactive protein, 280 mg/L). Neutropenic septic shock with right middle lobe pneumonia was diagnosed. Therapy was commenced with fluid resuscitation, antibiotics (piperacillin/tazobactam, gentamicin, fluconazole, cotrimoxazole), and bone marrow stimulation (filgastrim). Spiral CT of the chest excluded pulmonary embolus. Echocardiography showed a dilated left ventricle with trivial mitral regurgitation and ejection fraction of 70%. Progressive hypoxemia (pH 7.37; PO2, 56 mm Hg; PCO2, 47 mm Hg; base excess, – 4; bicarbonate, 20 mmol/L) despite noninvasive ventilatory support required endotracheal intubation and mechanical ventilation. Transesophageal Doppler analysis revealed a baseline cardiac output of 4.5 L/min (cardiac index, 2.8 L/min/m2) with stroke volume (SV) of 40 mL. Within 1 h of admission to the ICU, atrial fibrillation developed with a ventricular rate of 150 beats/min. Chemical (IV magnesium sulfate and amiodarone) and electrical cardioversion failed to re-establish sinus rhythm, although rate declined to 105 beats/min. Over the following 4 h, cardiac output declined (to 2.8 L/min; cardiac index, 1.6 L/min/m2; SV, 26 mL) despite a central venous pressure (CVP) of 15 mm Hg. Oliguria and acidemia ensued (pH 7.25; PCO2, 52 mm Hg; PO2, 74 mm Hg; base excess, – 5; bicarbonate, 20 mmol/L) necessitating continuous venovenous hemofiltration. Over the following 8 h, increasing infusions of epinephrine (rising to a maximum of 56 µg/min) and colloid challenges (totaling 4 L) failed to significantly improve mean arterial pressure (MAP) [55 mm Hg] or cardiac output (3.1 L/min; cardiac index, 1.9 L/min/m2; SV, 26 mL; CVP, 26 mm Hg). A repeat echocardiogram showed poor left ventricular contractility with biventricular dilatation and poor ejection fraction (40%). An infusion of GIK (30% glucose with 50 units of actrapid insulin and 80 mmol/L potassium at 1.5 mL/kg/h) was associated with a dramatic increase in cardiac output (Fig 1 ; Table 1 ). Within 4 h of commencing GIK, it was possible to start weaning the epinephrine infusion; the greatest reduction occurred in the first 14 h (from 56 to 16 µg/min), with an infusion rate of just 6 µg/min at 72 h, when GIK was ceased, and cessation of epinephrine at 130 h (MAP, 72 mm Hg; cardiac output, 5.5 L/min; SV, 44 mL). The patient required no further pressor support for the next 4 days. Glucose concentrations throughout the ICU stay ranged from 5 to 8 mmol/L. Ten days after hospital admission, systemic Staphylococcal infection and candidiasis developed, resulting in death.


Figure 1
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  		Figure 1.. GIK infusion in patient 1: increase in cardiac output with reduction in epinephrine dose within hours of commencing GIK. ITU = ICU.

 

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  		Table 1.. Hemodynamics and Glucose Levels Before and After GIK Administration in Patient 1

 

   Case 2
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 Abstract
 Introduction
 Case 1
 Case 2
Discussion
 References
 
A 23-year-old man with a history of paroxysmal nocturnal hemoglobinuria was admitted to the ICU with neutropenic septic shock. He had received cyclosporine, mycophenolate mofetil, and bone marrow stimulating factors (granulocyte-colony stimulating factor) prior to haploidentical bone marrow transplantation administered 2 days earlier. Two years earlier, Budd Chiari syndrome had been treated with an intrahepatic portosystemic shunt insertion.

On the day of hospital admission, the patient collapsed with loss of consciousness, requiring endotracheal intubation and mechanical ventilation. He was febrile (39°C), peripherally dilated, jaundiced, tachycardic (130 beats/min), and hypotensive (BP, 90/50 mm Hg). Oxygen saturations were 95% (fraction of inspired oxygen of 60%), and bibasal lobar collapse and consolidation was confirmed on chest radiography. The patient had profound metabolic acidosis (pH 6.82; PCO2, 39 mm Hg; PO2, 102 mm Hg; base excess, – 23), pancytopenia, coagulopathy, deranged urinary and liver biochemistry (WBC, 0.2 x 109/L; hemoglobin, 7.8 g/dL; platelets, 57 x 109/L; international normalized ratio, 2; APTT, 85 s; TT, 15 s; urea, 111 mmol/L; creatinine not measurable; sodium, 159 mmol/L; potassium, 3.5 mmol/L; bilirubin, 562 µmol/L; alkaline phosphatase, 496 IU/L; alanine aminotransferase, 206 IU/L; albumin, 30 g/dL; calcium, 2.2 mmol/L; phosphate, 2.4 mmol/L; C-reactive protein, 190 mg/dL; glucose, 7.0 mmol/L). An ECG showed no acute changes, and results of CT of the head were normal. A diagnosis of neutropenic septic shock secondary to hospital-acquired pneumonia was made. Broad-spectrum antimicrobials (teicoplanin, ceftazidime, amphotericin, and foscarnet) were immediately commenced, and the patient was resuscitated with sodium bicarbonate (8.4%) colloid, crystalloid, and blood products (totaling 6.5 L). Despite this, the patient remained hypotensive (80/40 mm Hg), tachycardic (110 beats/min), and anuric. Treatment was commenced with norepinephrine, and continuous venovenous hemofiltration was initiated. Over 4 h, norepinephrine doses were steadily increased to a maximum of 11 µg/min, maintaining a MAP of > 60 mm Hg (cardiac output, 3.9 L/min; cardiac index, 2 L/min/m2; SV, 49 mL). Over the next 6 h, the patient again became progressively hypotensive, with a corresponding decline in cardiac output (MAP, 45 mm Hg; cardiac output, < 2 L/min; cardiac index, < 1 L/min/m2; SV, 55 mL) and required a further 3 L of colloid. Norepinephrine was replaced with escalating epinephrine infusion, reaching a maximum of 20 µg/min at 6 h. MAP and cardiac output remained poor (50 mm Hg; cardiac output, < 2 L/min; cardiac index, < 1 L/min/m2; SV, 40 mL). Echocardiography showed a dilated right ventricle with normal left ventricular dimensions. Pulmonary embolism was excluded by CT pulmonary angiography. In view of the low cardiac output and poor response to epinephrine and colloid, high-dose GIK was commenced (30% glucose with 50 units of actrapid insulin and 80 mmol of potassium at 1.5 mL/kg/h). This was associated with a significant rise in cardiac output, with a corresponding increase in MAP (Fig 2 ; Table 2 ). Epinephrine was weaned to cessation within 8 h of commencing GIK. Acid-base balance had normalized, but the patient remained oliguric. The GIK infusion was stopped within 18 h of initiation. The patient remained hemodynamically stable and maintained a cardiac output from 5 to 6 L/min, with a MAP of > 70 mm Hg for the following 8 days. Glucose levels were maintained from 6 to 8 mmol/L throughout hospital admission, including the period of the GIK infusion. An abdominal ultrasound scan showed partial obstruction of the portosystemic shunt. Shunt revision was planned for the following day. However, recurrent hypotension with a high-output circulation (cardiac output, 10 L/min; cardiac index, 5.2 L/min/m2; MAP, 50 mm Hg; SV, 80 mL) led to readministration of norepinephrine. Resistant thrombocytopenia (platelets, 4 x 109/L) and markedly deranged coagulation (APTT, 50 s; TT, 18 s; PT, 30 s) resulted in pulmonary and GI hemorrhage with respiratory failure (PaO2, 45 mm Hg; PaCO2, 53 mm Hg; fraction of inspired oxygen, 60%; respiratory rate, 40 breaths/min; tidal volume, 200 to 300 mL; pressure support, 20 cm H2O; positive end-expiratory pressure, 10 cm H2O). With full family consent, treatment was withdrawn and the patient died. In both cases, activated protein C, corticosteroids, vasopressin, or other adjuvant therapies for sepsis were not administered.


Figure 2
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  		Figure 2.. GIK infusion in patient 2: sustained improvement in cardiac output and decrease in epinephrine dose following introduction of high-dose GIK. See Figure 1 legend for definition of abbreviation.

 

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  		Table 2.. Hemodynamics and Glucose Levels Before and After GIK Administration in Patient 2

 

   Discussion
TOP
 Abstract
 Introduction
 Case 1
 Case 2
 Discussion
References
 
We have described two cases of neutropenic septic shock in which the administration of a high-dose GIK infusion was temporally associated with an improvement in hemodynamic profile, permitting cessation of inotropic support. Septic shock and the systemic inflammatory response is characterized by reversible myocardial depression, which can prove resistant to catecholamine and fluid administration.123 Circulating "myocardial depressant factor"—probably representing the synergistic effects of tumor necrosis factor (TNF)-{alpha}, interleukin (IL)-1ß, other cytokines, and nitric oxide4—is implicated in pathogenesis. Macrovascular myocardial ischemia and hypoperfusion are unlikely contributors.56

GIK infusions were first proposed as a metabolic treatment for acute myocardial ischemia in the 1960s, with recent renewed interest in its use in the context of acute myocardial infarction and cardiac surgery.7 Acute myocardial ischemia results in an increased collateral blood flow and elevates circulating catecholamine levels as a result of physiologic stress. Depletion of carbohydrate reserves occurs in parallel with a switch to the use of less efficient energy substrates such as free fatty acids (FFAs), lactic acid, amino acids, and ketone bodies. These provide lower adenosine triphosphate yield per metabolized oxygen molecule. "Forcing" the ischemic myocardium to use glucose (through GIK administration) may thus improve the metabolic state of the myocardium when oxygen and fuel delivery is limited. Such metabolic support may also limit reperfusion injury.8 Indeed, GIK improves myocardial perfusion and left ventricular function in diabetic patients, improves systolic function in patients with stable coronary artery disease, and ischemically preconditions the myocardium.91011 Meta-analysis12 suggest GIK use to be associated with reduced in-hospital mortality after acute myocardial infarction, a conclusion supported by one large randomized control study.13 Further randomized control studies,141516 however, have shown no significant benefit in salvaging myocardium or improving mortality following primary angioplasty. In a randomized controlled trial17 in patients treated for myocardial infarction, high-dose GIK had neutral effects on mortality, cardiac arrest, and cardiogenic shock. Meanwhile, GIK seems associated with dramatic increases in cardiac index with reduced inotropic support in the context of coronary artery bypass surgery.101118

Few studies have, however, addressed the role of GIK in septic myocardial depression. Mauritz et al19 showed that GIK (70%; 1 g/kg body weight; insulin, 1.5 units/kg; potassium, 10 mmol/L) improved MAP and cardiac and stroke work indexes in 15 patients with hypodynamic septic shock secondary to peritonitis. Similarly, Bronsveld et al20 showed a 20-min GIK infusion (glucose, 50%; 1 g/kg body weight; insulin, 1.5 µ/kg; potassium, 10 mmol/L) to significantly improve left ventricular stroke work indexes in 6 patients with fluid- and pressor-resistant hypodynamic septic shock. There were similar nonsignificant improvements in nine hyperdynamic patients. Our reports are thus consistent with those previously described.

Insulin decreases circulating levels of IL-1ß, IL-6, migration inhibitory factor, TNF-{alpha}, and increases levels of IL- 4 and IL-10 in thermally injured rats. In lipopolysaccharide-treated animals, insulin suppresses TNF-{alpha} in a dose-dependant manner. Furthermore, insulin reduces proinflammatory and increases antiinflammatory cytosolic signal transduction constituents.21 Insulin has been shown to enhance production of endothelial nitric oxide, suppress superoxide anion generation, and inhibit myocardial apoptotic death.22 Hence insulin appears to have antiinflammatory effects. Because of the local effects of insulin and through its suppression of FFAs, insulin infusions cause an increase in glucose uptake in both dysfunctional and normal myocardial regions.2324 Increased FFA levels are toxic to ischemic myocardium and are associated with increased membrane damage, arrhythmias, and decreased cardiac function.25 The anti-FFA effects of GIK may be especially beneficial in patients with high circulating levels of catecholamines, which increases serum FFA levels. Insulin infusions also increase the generation of adenosine triphosphate production from glycolysis.26 In the resting fasting state, glucose only accounts for approximately 30% of the energy production of the heart; suppression of FFA by insulin allows the myocardium to increase the utilization of glucose, which is a more efficient energy source.27 Why GIK infusions are beneficial in septic shock is unclear but is likely to involve a combination of antiinflammatory and metabolic mechanisms.

Why GIK improved hemodynamics in our two patients is unclear. It is conceivable that patient 1 had unidentified coronary artery disease, and in a high output state myocardial energy demand was far greater than supply, hence supplementing the myocardium with glucose improved cardiac output. Although, there was no clear reduction in inotrope requirements on commencing antibiotics, it remains possible that some of the decrease in inotrope dose merely represented a response to antibiotic therapy. Both patients were adequately volume resuscitated by colloid, and GIK contributed to < 100 mL/h of the total volume load. This coupled with the magnitude and rate of response to GIK suggests that the hemodynamic improvements were unrelated to a simple volume-loading effect. "Tight" normoglycemic control is associated with improved mortality in intensive care28 and may have contributed to prolonged survival in the two described patients. However, mean and range of glucose levels were similar before and during GIK administration, suggesting a specific role for the combination of glucose, insulin, and potassium on the improvement in hemodynamic profile and withdrawal of inotropes.

We have described two cases of pressor-resistant hypodynamic septic shock that were possibly reversed by GIK. The mechanism for this is unclear. Further evaluation of GIK in the management of pressor-resistant hypodynamic septic shock is necessary.


   Footnotes
 
Abbreviations: APTT = activated thromboplastin time; CVP = central venous pressure; FFA = free fatty acid; GIK = glucose-insulin and potassium; IL = interleukin; MAP = mean arterial pressure; PT = prothrombin time; SV = stroke volume; TNF = tumor necrosis factor; TT = thrombin time

Received for publication October 23, 2005. Accepted for publication December 3, 2005.


   References
TOP
 Abstract
 Introduction
 Case 1
 Case 2
 Discussion
 References
 

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M. Y. Rady, S. S. Hamdulay, H. Montgomery, A. Al-Khafaji, J. M. Marchant, A. B. Chang, and B. K. Rubin
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