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Tourniquets are applied around upper or lower extremities to eliminate intraoperative bleeding and thereby provide better operative conditions. Unfortunately, the tourniquet is not physiologic and is associated with a number of disadvantages ( Table 61-7 ). The use of a tourniquet in patients with sickle cell disease remains a source of controversy. Concerns over precipitating a sickle cell crisis by the low oxygen concentration in the ischemic limb are weighed against decreased blood loss and the need for a bloodless field. Little research exists on this topic, but one series reported the safe use of a tourniquet in 12 children with sickle cell disease with no consequent sickle-related crises or complications.[204] If a tourniquet is used, adequate hydration, warmth, and blood volume must be maintained.
Mitochondrial partial pressure of oxygen decreases to zero within 8 minutes of inflating a tourniquet. Anaerobic metabolism then begins. Decrease of nicotinamide adenine dinucleotide and creatine phosphate stores in muscle occurs over the next 30 to 60 minutes.[205] Cellular acidosis (pH < 6.5) rapidly ensues.[205] [206] Hypoxia and acidosis result in the release of myoglobin,[207] intracellular enzymes, and potassium.[208] Thromboxane is released locally, causing disruption of endothelial integrity.[209] Tissue edema develops if tourniquets are inflated more than 60 minutes; closure of ankle incisions may then be difficult.[210] The limb loses heat and may approach room temperature with time. Injury to muscle beneath the tourniquet may delay rehabilitation.[211]
With deflation of the tourniquet and reperfusion of the extremity, a washout of metabolic by-products occurs.[212] A decrease in core body temperature of 0.7°C typically occurs within 90 seconds of deflation of a lower limb tourniquet,[213] [214] and venous oxygen saturation[215] may fall 20% in 30 to 60 seconds. Increases in end-tidal carbon dioxide typically occur,[216] but decreases in arterial oxygen saturation are uncommon unless significant pulmonary shunting exists.[217]
| Neurologic Effects |
| Abolition of somatosensory evoked potentials and nerve conduction occurs within 30 minutes |
| Application for more than 60 minutes causes tourniquet pain and hypertension |
| Application for more than 2 hours may result in postoperative neurapraxia |
| Evidence of nerve injury may occur at a skin level underlying the edge of the tourniquet |
| Muscle Changes |
| Cellular hypoxia develops within 8 minutes |
| Cellular creatine level declines |
| Progressive cellular acidosis occurs |
| Endothelial capillary leak develops after 2 hours |
| Limb becomes progressively colder |
| Systemic Effects of Tourniquet Inflation |
| Arterial and pulmonary artery pressures become elevated, although this effect is usually slight to moderate if only one limb is occluded |
| Systemic Effects of Tourniquet Release |
| Transient fall in core temperature[214] |
| Transient metabolic acidosis |
| Transient fall in central venous oxygen tension (but systemic hypoxemia unusual) |
| Release of acid metabolites into central circulation (e.g., thromboxane) |
| Transient fall in pulmonary and systemic arterial pressures |
| Transient increase in end-tidal carbon dioxide |
| Increased oxygen consumption[286] |
The causes of hemodynamic responses are the initial inflation of the tourniquet, subsequent prolonged tourniquet inflation, and an immediate response after tourniquet deflation ( Fig. 61-7 ).
Inflation of the tourniquet and exsanguination of the limb result in an expansion of central venous blood volume and a theoretical rise in peripheral vascular resistance. In ordinary practice, this results in small increases in central venous or arterial pressures.[218] [219] However, patients with extensive varicose veins or poor ventricular compliance may experience considerable increases in pulmonary artery pressure (see Fig. 61-7 ). Bilateral, simultaneous tourniquet inflation of the lower extremities may result in significant elevations in central venous pressure.[218] [220]
Deflation of the tourniquet with reperfusion of the ischemic limb is frequently associated with decreases in central venous and arterial pressures. [221] These decreases can be profound (see Fig. 61-7 ) and have resulted in cardiac arrests.[222] Contributing factors include sudden reduction in peripheral vascular resistance with
Figure 61-7
The hemodynamic effect of thigh tourniquet inflation
(single bar) and deflation (double
bar) in an 86-year-old man with hypertension undergoing total-knee replacement.
Notice the changes in pulmonary and systemic artery pressures with inflation and
deflation of the tourniquet. The persistent elevation in pulmonary artery pressure
after reinflation of the tourniquet after deflation (after third
bar) may represent transient myocardial dysfunction.
Between 45 and 60 minutes after tourniquet inflation, patients under general anesthesia may develop systemic hypertension.[223] The reason for this rather consistent timing is not entirely clear, but it may reflect a critical level of cellular ischemia in the muscle or nerve. Attempts to reduce blood pressure by deepening anesthesia are not always successful, and vasodilators such as hydralazine, nifedipine, or labetalol may be necessary.[223]
Patients receiving spinal or epidural anesthesia may develop a poorly defined aching or burning sensation in the distal extremity about 1 hour after tourniquet inflation.[224] [225] Attempts to relieve "tourniquet pain" with intravenous narcotics are not always successful. Tourniquet pain may, however, be relieved by deflating the tourniquet for 10 to 15 minutes and then reinflating it. This correlates with correction of cellular acidosis.[226] Our experience has demonstrated that a complete brachial plexus block using long-acting local anesthetics is not associated with tourniquet pain for as long as 3 to 4 hours. Neither stellate ganglion nor intercostobrachial nerve blocks are effective in relieving tourniquet pain of the upper extremity.[227] These observations taken together suggest that tourniquet pain may be related in some manner to the quality or intensity of somatic neural blockade.[227] Experience with spinal anesthesia also suggests that the intensity of blockade may be more important than the anesthetic level in preventing tourniquet pain, because isobaric spinal anesthesia has a lower incidence of tourniquet pain than hyperbaric spinal anesthesia. [228]
Neurologic problems may occur when tourniquets are inflated for long periods (>2 hours) or when excessive inflation pressures are used. A shear force is applied to nerve trunks at the edges of the tourniquet.[229] Within 30 minutes of inflating a tourniquet, nerve conduction ceases.[230] [231]
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