• No results found

Shell / Skin: Composed of skin, subcutaneous fat, represents barrier between previous 2 compartments and environments

COMPLICATIONS OF THE HEAD-ELEVATED POSITIONS Postural hypotension

A) Iatrogenic causes: During anesthesia, hyperthermia results from a) active warming of patients (particularly pediatric patients) b) During

III. Shell / Skin: Composed of skin, subcutaneous fat, represents barrier between previous 2 compartments and environments

and acts as an insulator to the body.

Temperature changes under general anesthesia follows 3 phases:

Phase I% :% Internal redistribution Phase II% :% Thermal imbalance

Phase III % :% Plateau phase or Rewarming phase Phase I: Internal redistribution

• It results from vasodilatory effects of anesthetics mainly caused by reducing the threshold for vasoconstriction to a level below the current body temperature leading to opening of AV shunts.

This increases size of central compartment. There is decrease in metabolic heat production caused by anesthesia which reduces the amount of energy available to compensate for increase in central compartment.

• Rapid core temperature decreases by 0.5 – 1.5o C during first hour due to redistribution of core heat to periphery. This decreases core temperature but mean body temperature and body heat content is unchanged.

Phase II: Thermal imbalance

• Core temperature decreases in a slow linear fashion for 2 – 3 hours.

This is because heat loss >metabolic heat production. The mean loss is 0.5 – 1o C/ hr.

• Anesthesia contributes to decrease in production by limiting

muscular activity, decrease in metabolic rate and diminishing work of breathing.

• Convection and radiation > 85% heat loss.

conduction and evaporation > 15%, but 25% in infants

• Respiratory losses 5 – 10% of total heat loss. But it represents 1/3 of total heat loss in infants because minute ventilation on per kg basis is higher than in adults.

Phase III: Plateau phase or re-warming phase

• It occurs after 3-4 hours of anesthesia and virtually remains constant for the duration of surgery. It is a steady state where heat

production = heat loss.

• It is associated with peripheral thermoregulatory vasoconstriction when the core temperature is between 33 – 35o C.

• Another factor which contributes to plateau is the restriction of metabolic heat produced to core compartment in contrast to

peripheral tissue which continues to decrease the temperature since heat is no longer supplied by central compartment.

• In comparison to adults, infants and children replaced this steady state with rewarming phase. GA decreases heat production by inhibiting muscular activity and decreases metabolic rate, but there is simultaneous increase in oxygen consumption, CO2 production and nor adrenaline level in infants because of occurrence of non

shivering thermogenesis. Infants differ from adults in that

intraoperative thermoregulatory responses are sufficiently effective to increase central temperature significantly despite constant ambient temperature.

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TEMPERATURE REGULATION DURING REGIONAL ANESTHESIA

• Spinal and epidural anesthesia can have several effects on thermoregulation.

• The vasoconstriction and shivering thresholds are decrease in regional anesthesia, which suggests an alteration in central control because of altered thermal input i.e. an apparent elevation of leg temperature and administration of opioids and sedatives. The perception of temperature is largely determined by skin rather than core temperature. In regional anesthesia there is core hypothermia which increase temperature in the periphery, below the level of block. The result is continued perception of warmth accompanied by autonomic

thermoregulatory response including shivering which is more pronounced in the area which is unblocked.

• This mechanism of heat loss persist in the regional anesthesia until the block wears off, whereas in general anesthesia patients begin to rewarm immediately on emergence.

• Shivering with epidural is less vigorous than compared to after GA and therefore has fewer hemodynamic metabolic

consequence.

EFFECTS OF ANESTHETIC DRUGS ON THERMOREGULATION 1).Inhalation agents:

• All inhalational agents augment inter-threshold range in dose dependent manner.

• N2O →↓ in shivering thermogenesis.

• Halothane ↓ thermoregulatory threshold to 34.4o C at 1.3 MAC.

In children – anaesthetized with 1 MAC with 7-% N2O with oxygen ↓ thermoregulatory threshold to 35.8o C.

• Enflurane – In adults with 1.3% or (0.77 MAC). Thermoregulatory threshold (TRT) for vasoconstriction was 35.1o without and 35.5o C with painful stimulation. 1 – 12 years, 1.67% or 1 adult MAC in oxygen with caudal bupivacaine caused profound depression of TRT for vasoconstriction, failing to vasoconstriction even when

temperature is 33.9o C.

• Isoflurane – TRT is inversely proportional to inhaled concentration and decreases by about 0.3o C for every 1% increase in end tidal inhaled concentration.

2). IV agents:

• Midazolam minimally impairs TRT.

• Ketamine minimally alters in dose dependent manner.

Muscle relaxants reduce capacity of body to respond to hypothermia even though slight decrease in oxygen consumption (2%) occurs in normothermic and hypothermic patient with pancuronium.

3). Opioids:

• Decreases the vasoconstriction and shivering thresholds.

• Alfentanil – slight increase in sweating threshold and linear decrease in vasoconstriction and shivering thresholds.

• Meperidine – has antishivering action which is due to disproportionate drop in shivering threshold.

• Tramadol – has slight effect on thermoregulatory control.

4). Adjuvants:

• Clonidine – decreases shivering by lowering vasoconstriction and shivering thresholds.

• Intraoperative tourniquets induces hyperthermia, due to reduction in peripheral compartment and containment of heat in core

compartment, which explains drop in core temperature when vascular clamp is withdrawn.

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HYPOTHERMIA

• Usually defined as body temperature less than 36o C.

Causes of hypothermia:

1. OT temperature – most of OT temperature is between 18 – 21o C, increased temperature produces perspiration and increase chances of microbial transfer and seeding of wounds. Patients looses heat when temperature is < 21o C.

2. Administration of cold blood or IV fluids.

3. Prolonged surgery.

4. Intra abdominal surgery or intrathoracic surgery due to exposure of large viscera, body cavities.

5. Use of repeated large volumes of irrigating fluids.

6. Direct effects of anesthetic drugs which depress bodyʼs feedback for maintenance of thermoregulation. Muscle relaxants impede thermogenesis by eliminating shivering.

Effects of hypothermia:

• Inadvertent hypothermia can have a variety of manifestations.

• CNS – altered mental status, disturbances in gait and speech, sluggish deep tendon reflexes, slow and shallow respiratory pattern. Increase in cerebral vascular resistance (CVR).

• CBF is proportional to decrease in metabolic rate because of autoregulatory CVR.

• AV PO2 remains constant and venous lactate doesnʼt increase.

• Cerebral function is well maintained until core temperature is equivalent to 33o C but consciousness is lost when temperature is < 28o C.

• Primitive reflexes like gag, cough, papillary constriction and monosynaptic spinal reflexes remain intact until 25o C.

• Nerve conduction decreases but tone of peripheral muscle increase at 26o C.

• CVS – Cardiac rhythm disturbances -% SVT

AF

Ectopics

Heart block

Conduction disorders

Suppression of higher pacemakers

Hypotension and decreased cardiac output

Terminal events – VF or asystole.

• Hematologic: Left shift of ODC which impede oxygen delivery and leading to cellular hypoxia and metabolic acidosis. Increases blood viscosity.

• Can hinder homeostasis with sequestration of platelets which can lead to DIC.

• Metabolic: Decreases metabolic rate by 5 – 8% per degree C to approximately ½ of normal rate at 28o C. Decrease tissue perfusion

→ can lead to metabolic acidosis → lipolysis → increased FFA → glucose use → hypoglycemia. Increases tissue oxygen consumption by 400 – 500%.

• Pulmonary: Respiratory strength is decreased at 33o C. Increased PVR, MVV which is required for additional oxygen demand.

• Decreases hepatic blood flow – decreases the liver function, decreases metabolism and excretion of drugs.

• Decreases renal blood flow – renal perfusion decreases, GFR decrease, tubular insufficiency.

• ʻCold diuresisʼ Treatment:

• Warmed IV fluids, heated humidified gases

supporting treatment of cardiac renal, metabolic consequences Inadvertent hypothermia can best be corrected with gradual spontaneous rewarming with blankets in a warm room.

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POST ANESTHETIC SHIVERING

• Shivering is common complications occurring in 40% of patient during post anesthetic recovery. It is considered as a normal thermoregulatory shivering only when

• Mean body temperature is below threshold for shivering

• Tremor is preceded by peripheral cutaneous vasoconstriction.

• Tremor patterns match those produced by centrally mediated shivering.

• The cause for tremors has been attributed to uninhibited spinal reflexes, pain, decreased sympathetic activity, pyrogen release, adrenal suppression, respiratory alkalosis and most commonly due to intraoperative hypothermia.

EMG show 2 patterns for tremors.

1). Tonic pattern typically having 4- 8 cycles / min. Waxing and waning component.

2). Phasic pattern having 4 – 7 Hz of bursting pattern which resembles clonus.

Effect: 25% of post. Op patient reach a core temperature of 38o C and 50% reach 38.4o C and this will eventually lead to increase in thermoregulatory set point.

Prevention:

• PAS is defense mechanism against reduction of core

temperature, so it should not be prevented, rather warming of patient should be undertaken than administering medication to inhibit it.

1. PAS can be treated with skin surface warming because the regulatory system will tolerate more core hypothermia when cutaneous warm input is augmented.

2 factors contribute to rapid intra op. transfer of heat from periphery to core.

• Vasodilatation induced by central inhibition of thermoregulatory control.

• GA itself induces peripherally mediated vasodilatation which facilitates intra-compartmental transfer of heat.

2. Cutaneous heat loss can be decreased by covering the skin with surgical drapes which decreases heat loss by 30%.

3. Radiant heat lamps can be used during preparation and catheter placement.

4. OT room temperature can be increased to 25o C until the patient is fully draped.

5. Forced air system can transfer more than 50 W across skin surface there by rapidly increasing the body temperature (Bair Hugger).

6. Heated humidifiers and airway heating is effective in rewarming children and infants rather than adults who help in retaining the heat and moisture within respiratory system.

7. Fluid warmers- 1 L of crystalloid solution at room temperature or 1 point of refrigerated blood will decrease the mean body temperature by 0.25o C. So fluids or blood should be warm.

8. Water circulating warming blankets may be of value when placed on top of patient. The temperature of water should not exceed 40o C.

Treatment of hypothermia and shivering in PACU:

Supplemental oxygen until patient are fully warm.

Stop shivering by giving pharmacological agents Inj. Meperidine 25 mg IV

Inj. Clonidine 75 µg IV Inj. Ketonserin 10 mg IV

• Cutaneous heat source – forced air system, warming blankets,

radiant heat lamps. Paralysis and ventilation in severely hypothermic sick patients.

HYPERTHERMIA:

• Hyperthermia is defined as increase in body core temperature higher than 38.3o C whereas fever is an endogenously triggered process with metabolic and functional changes that alter hypothalamic set point.

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Pathophysiology of hyperthermia:

• The primary injury in hyperthermia is direct cell toxicity above 42o C (critical thermal maximum) cell function deteriorates with cessation of mitochondrial activity, alteration in cellular enzyme function and loss of cell membrane integrity. Irreversible

changes of coma, cerebral hypoxia, acidosis, rhabdomyolysis, dehydratation and organ damage can occur leading to death.

The manifestation of hyperthermia on organ function are – 1).% CVS % -Vasodilatation

% % -Increased heart rate 10 beats / o C rise in temp.

% % -Increased stroke volume

% % -Decreased venous return

% % -Hypotension

• Oxygen demand is increased initially leading to increase in cardiac output. Later increase in oxygen extraction by tissue outstrips the supply.

• Myocardial damage occur in the form of myocardial

haemorrhage, dysrrhythmias, heart failure and demand induced ischemia.

Metabolic:

• 1o C rise in body temperature increases BMR by 7% with a parallel increase in oxygen consumption, CO2 production and fluid and nutrition requirements. This increased systemic demands can impose a great burden on marginal CVS.

Respiratory:

• Decreases tidal volume

• Increases respiratory rate

• Increased ventilatory response to hypoxemia & hypercapnea

• Increased hypoxic pulmonary vasoconstriction

• Shift of ODC to right

Endocrine:

• Temperature regulation has physiologic priority over maintenance of salt and water balance. Sweating continues in phase of severe dehydration and salt loss leading to circulatory failure.

• There is increase in ADH, aldosterone, growth hormone, corticosteroids and thyroid hormone.

CNS:

• Seizures

• Delirium

• Coma

• Death

• Survivors show ataxia and dysarthria.

GIT

• Bleeding from gut

• Acute liver failure Hematologic system %

• Coagulopathy

• DIC

Muscle – Degeneration and necrosis occurs leading to rhabdomyolysis and myoglobin release.

Causes of hyperthermia "

• Exogenous Endogenous Exogenous

• Draping the patient

• High humidity

• Elevated room temp.

• Use of warm blankets, heated mattress or blood warmers.

• Circle system with soda lime

• Heated humidifiers

• Large operating room lights

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Endogenous:

• Malignant hyperthermia

• Neuroleptic malignant syndrome

Drug Induced

Surgical wound infection Phlebitis

Transfusion

Febrile reaction (pyrogens, cell debris endotoxins) Incompatibility

Reactions against leukocytes, platelets

Endocrinopathy

Impairment of sweating (atropine, scopolamine)

Inflammatory response

Systemic inflammatory disease Tissue trauma and inflammation Gastric content aspiration

Miscellaneous Methyl methacrylate Sclerosing solution

I). MALIGNANT HYPERTHERMIA:

Is a rare disorder that appears to involve excessive release of Ca from sarcoplasmic reticulum in response to anesthetic agents. The increase in Ca initiates a severe muscle hypermetabolism. It is a autosomal dominant disorder, hence a positive family history is always present.

Incidence % :% Adults 1: 50,000

% % % Children 1: 15,000

• Onset: Is acute during induction with inhalation anesthesia or with

administration of scoline but recurrence of the syndrome can occur within first 24 to 36 hours.

• MH can be diagnosed by muscle biopsy or by caffeine halothane contracture test.

• Triggering agents – halogenated general anesthetic like ether, halothane, cyclopropane, methoxyflurane, enflurane, isoflurane, desflurane

sevoflurane.

• Non depolarizing muscle relaxants like scoline Signs and symptoms are:

Hypermetabolism

% Increased CO2 production

% Increased O2 consumption

% Metabolic acidosis

% Cyanosis

Increased sympathetic activity

• Tachycardia

Initial hypertension Arrhythmias

Muscle damage

% Masseter spasm

% Generalized rigidity

% Elevated serum creatinine Kinase

% Hyperkalemia

% Hypophosphatemia

% Myoglobinuria

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• Hyperthermia

Body temperature often exceeds 41o C and may be as high as 45o C.

• MH of anesthesia has high mortality rate upto 70%. But with advent of Dtc it has dropped to 10% which is a muscle relaxant that inhibits the release of calcium from sarcoplasmic reticulum.

Other important measures include prompt interruption of anesthesia, correction of hypoxia and metabolic disturbances and CVS support.

• Physical cooling with ice packs, core cooling with parenteral fluids have been advocated.

DIAGNOSIS:

• Monitoring of body temperature should be mandatory in all patients undergoing general anesthesia. The 4 most common temperature transducers are

Thermocouple Thermistor

Infrared tympanic thermometer Liquid crystal thermometer

Once hyperthermia is established.

• Evaluate patient history, physical examination and rule out predisposing condition.

• Evaluate drugs which might trigger.

• Assess signs and symptoms Lab Tests

-% Electrolytes and lactate

-% Plasma free Hb or heptoglobin -% Urine myoglobin

-% Creatinine kinase -% Antiglobulin test -% Blood Cultures -% Compliment levels

-% Complete blood count and clotting time

Management:

• Involves promoting heat loss and reducing heat production.

• Temperature < 39oC Look for cause

Remove covers and warming devices Discontinued triggering agents

Discontinued blood transfusion if any.

• Temperature > 39o C or 0.5o C / 15 min.

1) Give 100% oxygen.

2) Initiate active cooling measures by blowing cool air, wet drapers, reduce OT temp. Ice packs, ice solution lavage into stomach, rectum and operative sites, peritoneal dialysis.

3) Consider terminating surgery.

4) Send for blood analysis.

• Temperature equivalent 40o C.

• Patient should be paralysed and mechanically ventilated using high minute volume to eliminate CO2.

• Dantrolene should be administered.

Temperature > 40o C

• Hemofiltration should be considered.

• Other symptomatic measures Other symptomatic measures:

• Antiseizures medication like phenytoin can be given prophylactically once temp. pouches 39o C. if convulsion are present diazepam can be given.

• Renal function should be monitored with urine output maintained with fluid replacement or administration of mannitol, Frusemide.

• Cardiac dysrrhythmias can be caused by hyperkalemia and acidosis, so administration of glucose and insulin to correct hyperkalemia.

Bicarbonate can be given in severe acidosis Cacl2 can be given once hypocalcemia is confirmed.

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TEMPERATURE MONITORING:

The objective of temperature monitoring and perioperative.

Thermal management is to detect thermal disturbances and to maintain appropriate body temperature during anesthesia.

1. Core body temperature should be measured in most patient given GA for > 30 minutes, both to detect MH and to quantify hyper and hypothermia.

2. Temperature should be measured during regional anesthesia when changes in body temperature are intended.

3. Unless hypothermia is specially indicated efforts should be made to maintain intraoperative. Core temperature > 36o C.

Temperature monitoring involves –

Temperature probe selection.

Temperature monitoring site selection Temperature probes:

• Contact probes: The prototype is mercury thermometer. It has equalization time of 3-5 min.

• Use of mercury in glass is now economically unsound and represents a hazardous waste disposable problem.

Thermocouples and thermistors:

• Electrical thermometers are now commonly used for intraoperative monitoring of temperature.

• Electrical resistance of thermistor varies as a function of

temperature. Thermistors are fundamentally devices which are thermal sensitive resistances whose resistance changes with temperature.

• The principle of thermocouple is that if a circuit is made up of 2 dissimilar mental elements the current in the circuit will be directly proportional to temp. difference between 2 junctions of dissimilar metals. Here one of junction is always kept at

standard reference temp. (OO c) while other junction is located in temp. probe.

• Both have equilibration period of 20 – 30 sec.

• Liquid crystal thermometer – These are recently used thermometers for constant monitoring of skin temperature during anesthesia and into recovery phase. These devices use the thermal optic

transmission qualities of crystals. The temp. is read from adhesive strip as the colour of liquid crystal changes with temp.

• The liquid crystal material which is commonly a cholesteric base alters its molecular arrangement in response to temperature

variation. This configuration change permit some crystals to reflect or scatter light at given temp. While rest transmit light without aberration. This is used to monitor skin temp.

Advantages:

• Commercial kits are available

• Ease of application

• Continuous information output

• Simplicity in screening for MH.

Disadvantages

• Skin surface temp may not reflect core temp. accurately.

Infrared sensors

• Infrared temperature detectors look like otoscopes and are used to measure tympanic membrane temp.

Advantages:

• Response time is < 5 sec

• Very good index of core temp.

• Disposable thin plastic film cover reduces risk of infection.

Disadvantages

• Only intermittent spot checks can be made.

• Probe must be accurately placed aimed at tympanic membrane otherwise false low reading are a problem.

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ANATOMIC SITES FOR MONITORING

Oral: The classic location for oral location of temperature probe is sublingual on either side of frenulum.

The site is subjected to a number of external factors such as mouth breathing, crying, and recent ingestion of hot or cold food.

Skin: It is not a reliable index of core temp. because the degree of vasoconstriction or vasodilatation can significantly affect the

measurements obtained.

Forehead: It has received a lot of attention as an anatomic site for temperature monitoring because of introduction of liquid crystal temp. sensitive adhesive strips.

At normal OT room temperature heat lost from forehead is equal to heat lost from any other part of body with same surface area

exposed.

Rectal temp: It is an adequate indicator of core temp. during steady state. But drawback is that it seldom reflects actual core temperature in anaesthetized patient when temp changes are relatively rapid.

Can be used easily in infants than in adults. Major problem is of execution, patient discomfort.

Bladder: It is reliable index of core temp. But lower abdominal surgeries and irrigation with large amounts of fluids lowers the measured temp.

Nasopharynx: The temperature is close approximation with brain temp.

Measurements can be adversely affected by gas flow from ventilation resulting in lower temp. with high flows.

The danger of causing Epistaxis is a consideration especially in patient who are on anticoagulants.

Tympanic membrane: It approximates brain temp. better than any

Tympanic membrane: It approximates brain temp. better than any