ENDOCRINE EMERGENCIES IN ANAESTHESIA - PowerPoint Presentation

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ENDOCRINE EMERGENCIES

IN ANAESTHESIA

DR PAVANI KALYANAM

PROFESSOR

DEPARTMENT OF ANAESTHESIOLOGY OSMANIA GENERAL HOSPITALHYDERABAD

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ENDOCRINE SYSTEM

Growth and developmentMetabolismControl of body temperature, heart rate and blood pressureElectrolyte balance

Sexual function and reproduction

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ENDOCRINE EMERGENCIES

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ENDOCRINE

EMERGENCIES

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ENDOCRINE EMERGENCIES

ANAESTHESIOLOGISTS:

As first responders in emergency department

Optimize these patients for emergency surgery

Manage the crisis in the operative room

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DIABETIC EMERGENCIES

Hyperglycemic CrisisDiabetic Keto Acidosis(DKA)Hyperosmolar hyperglycemic stateHypoglycemia

DKA MC in T1D,often seen in T2Donset in a few hours HHSMC in T2Donset in days to weeksMortality-0.2-2%PRECIPITATING FACTORSNew onset diabetes(T1D-25%)Failure to take insulinFailure to increase insulin when requiredProvoking factorsInfection-pancreatitisAlcohol

TraumaMICVAPulmonary embolismDrugsSGLT2inhibitors-euglycemic DKAIncreased counterregulatory hormonesStressCOVID-19-6 fold increase in mortality

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HYPERGLYCEMIC CRISISPATHOGENESIS OF DKA AND HHS

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HYPERGLYCEMIC CRISIS CLINICAL FEATURES

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HYPERGLYCEMIC CRISIS

DIAGNOSTIC CRITERIAHyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar StateAidar R Gosmanov, M.D., Ph.D., F.A.C.E., Elvira O. Gosmanova, M.D., F.A.S.N.,, and Abbas E. Kitabchi, M.D., Ph.D., M.A.C.E.ADADKA

HHSBlood glucose>250mg%>600mg%HCO3<16mEq/L>20mEq/LPlasmapH

<7.3>7.3Non anion gap acidosis

+_Ketone bodies

+

_

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HYPERGLYCEMIC CRISIS

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HYPERGLYCEMIC CRISISDKA –life threatening emergency, requires prompt treatment, mortality -5%Anaesthesiologists Patient with DKA secondary to a surgical catastrophe and requiring immediate surgery

Acute abdomen—exclude DKA as causeTrauma ,cellulitis,diabetic foot for amputationDIFFERENTIAL DIAGNOSIS

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HYPERGLYCEMIC CRISIS Bedside monitoring of capillary glucose, ketones, blood gases, and electrolytes

MANAGEMENT

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HYPERGLYCEMIC CRISIS MANAGEMENT

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HYPERGLYCEMIC CRISIS

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HYPOGLYCEMIA

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HYPOGLYCEMIA

Sympathoadrenal

SweatingAnxietyTremorHungerPalpitationsNeuroglycopenic

Incoordination

ConfusionBlurring of vision

Severe hypoglycemia

Cardiac ischemia, cardiac arrhythmias,MI

Cognitive dysfunction,drowsiness(1-2mmol/l) coma (<1mmol/L)brain death .

Under anesthesia

Symptoms are masked.

Intraoperative

Nonspecific – hypertension, tachycardia, mydriasis

Depressed mental status, seizures, arrhythmias, SCD, hypoglycemic encephalopthy

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HYPOGLYCEMIA

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STRESS RESPONSE TO SURGERY

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NEUROENDOCRINE RESPONSE

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PHEOCHROMOCYTOMA AND PARAGANGLIOMA

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PHEOCHROMOCYTOMA AND PARAGANGLIOMAUndiagnosed pheochromocytoma under anaesthesiaSevere tachycardia, sweating, hypertension following induction, intubation and surgical manipulation of tumor.

Severe hypertension >220mmHg/120mmHg –CVA,CCFExclude other causes of intraoperative hypertension Deepening anaesthesia and beta blockers precipitates hemodynamic crisis –cardiac failure and acute pulmonary edema50% of deaths occur during anaesthesia and surgery and parturition

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PHEOCHROMOCYTOMAIf pheochromocytoma is suspected as underlying cause of hypertensive crisis the following treatment can be instituted

DRUGDOSEPhentolamine1mg IV boluses q 5-10min. Start infusion. 1-2mg/min and titrate to effect.Phenoxybenzamine1mg/kg infused over at least 2hrs.

NicardipineInfusion of 5-15 mg/hr, increase by 2.3mg/hr q15min to effect.NitroprussideInfuse initially with 0.5 to 1.5 mcg/kg/min to max 8mcg/kg/min over 1-3hrsNitroglycerine20 to 40mcg boluses q5-10mins to effect. Infusion 5-20mcg/min initial. Max dose 400mcg/min.

Propranolol1mg boluses to total 10mg.Esmolol

Load with 5-10mg boluses and infuse at 0.25 to 0.5mcg/kg/min.Labetolol5-10mg boluses q20-30minto maximum dose 150mg.

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PHEOCHROMOCYTOMAAfter ligation of adrenal vein during surgery- severe intractable hypotension.

Sudden drop in endogenous catecholamine levelsChronic downregulation of alpha-adrenergic receptorsIntravascular volume depletion.

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THYROTOXIC CRISIS

Rare -1-2% in hyperthyroid patients but mortality is 10-20%Delayed treatment-75% mortalityUnderlying thyrotoxicosis

CLINICAL FEATURESHypermetabolic stateRising temperatures(>102F)Tachycardia>140/minProfuse sweatingHypertension, Tachyarrhythmias(AF)High output cardiac failure, cardiovascular collapseCNS –agitation, delirium, seizures, comaLiver dysfunctionIncreasing ETCO2,exhaustion of soda limeElderly-apathetic thyroid stormPathophysiology - not clear.Beta1 receptors response to increased catecholamines in stressDisplacement of thyroid hormones

PRECIPITATING EVENTSSurgery, sepsis, burns, DKA,CVA, Parturition, status epilepticus,I131 therapy, iodinated contrast dyes

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THYROTOXIC CRISISMANAGEMENT

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THYROTOXIC CRISIS

MANAGEMENT

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HYPERCALCEMIC CRISISRare but life threatening

Commonly seen in hyperparathyroidism, malignancy  Commonly Calcium levels to be around 12 mg/dl prior to surgery.Indian J Endocrinol Metab. 2015 Jan-Feb; 19(1): 100–105.doi: 10.4103/2230-8210.131763PMCID: PMC4287752

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HYPERCALCEMIC CRISIS

Conservative management strategy -rapid intravascular volume expansion with isotonic saline solution @2.5-3ml/kg upto3-6L IN 24hBisphosphonates -Pamidronate 60mg IV when Ca>4.5mmol/LInfusion of phosphates to lower calcium levelsCalcitonin -3-4U/kg IV/SCDiuretics like frusemide to induce calciuresisDialysis -salvage therapy Semi-urgent or expeditious parathyroidectomy-optimize patient prior to surgery

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CARCINOID CRISISNeuroendocrine neoplasms from enterochromaffin or Kulchitsky

cellsSites – git, lungs, ovaries, testes, kidneys

Serotonin - diarrhea, vomiting, bronchospasm, hyperglycemia, drowsinessHistamine –bronchospasm, flushingBradykinin – vasomotor relaxation, severe hypotension, flushing5HT-fibrosis of endocardium-arrhythmias, tricuspid, pulmonary valvular lesionsClinical features of carcinoid syndromeCutaneous flushingDiarrheaWheezingSOB

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CARCINOID CRISISCarcinoid crisis –life threatening emergency

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CARCINOID CRISISMANAGEMENT

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ADDISONIAN CRISIS

Precipitating causesAny form of stress-even emotional

Acute infection(gastrointestinal)Septic shockTraumaSurgeryAbrupt withdrawal of long-term steroid therapyInadequate exogenous steroid replacement during stressEtomidateWaterhouse Friderichsen syndromeNormal cortisol 15-25mg/day of hydrocortisone or 5-7mg/day of prednisone

During stress/surgery75-150mg/day Serum cortisol-diurnal variation

8AM -5-23mcg/dl ,4PM-3-13mcg/dl Major surgery30-50mcg/dl,in ICU>60mcg/dl

Intake of >20mg/day of prednisone for>3weeks within the past one year-AI ,needs perioperative supplementation.

Adrenal insufficiency

Asymptomatic until 80-90% of gland nonfunctional or destroyed

Undiagnosed

D

iagnosed

Secondary

(Pituitary)

Primary

(Adrenal)

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ADDISONIAN CRISISIntake of >20mg/day of prednisone for>3weeks within the past one year-AI Needs

perioperative supplementation.Steroid/hydrocortisone supplementationType of surgeryDoseSuperficial surgery - Dental,biopsiesnone

Minor surgery - Inguinal hernia, colonoscopy25 mg IVModerate surgery - Cholecystectomy, colon resection50-75 mg IV, taper 1-2daysSevere surgery - Cardiovascular, liver, Whipple100-150 mg IV, taper 1-2 days Intensive care unit - Sepsis, shock

50-100 mg q 6-8 hrs for 2days to 1wk taper

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ADDISONIAN CRISIS

Life threatening condition-5-10 cases/100patient years with mortality 0.5/100 patient yrsSevere dehydrationIntractable hypotension out of proportion to precipitating illness and not responding to IV fluids and vasopressorsOTHER CLINICAL FEATURES

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ADDISONIAN CRISIS

Basal serum cortisol <20mcg/dlCortisol following ACTH stimulation test <20mcg/dlGlucocorticoid therapyHydrocortisone100mg iv followed by 25mg q6h or equivalent dose of dexamethasone 4mg iv followed by 2mg every 12 hours until vital signs are stabilized, and oral medication can be started.

Supportive therapyRehydration VasopressorsCorrection of electrolyte imbalancesHypoglycemia.Identify triggering event and treat accordingly.DIAGNOSISDIFFERENTIAL DIAGNOSISShock,Pituitary apoplexyAcute hypoglycemia

MANAGEMENT

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MYXEDEMA COMA

Incidence

Incidence0.22/million/yearElderly females with severe undiagnosed hypothyroidismMortality -30-50%Precipitating Factors

Stress of surgery

AnaesthesiaCold environmentInfection

Burns

Trauma

CHF

CVA

GI bleeding

Drugs

Clinical Features

Altered mental status

Hypothermia-GA

Hypotension-GA

Bradycardia-GA

Hyponatremia

Hypoglycemia

Hypoventilation

Hypercarbia

Pericardial effusion

Cardiogenic shock

Increased sensitivity to anesthetic drugs

Delayed recovery-GA

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MYXEDEMA COMA

No universal screening methods for thyroid functionAmerican Thyroid Association recommends screening at the age of 35years and every 5 years thereafter espPregnant womenElderly womenT1DMH/O neck irradiationLadenson PW, Singer PA, Ain KB, Bagchi N, Bigos ST, Levy EG, et al. American Thyroid Association guidelines for detection of thyroid dysfunction. Arch Intern Med. 2000;160:15735. [PubMed] [Google Scholar]

MANAGEMENTAirway -Mechanical ventilation -36-48hrsGlucocorticoid therapyHydrocortisone 50-100mg q8h or dexamethasone 2-4mg q12h

Thyroid hormone replacementLevothyroxine (T4)-IV 300-600mcg foll by 50-100mcg daily (one week)Liothyronine (T3)-IV 5-20mcg foll by 2.5-10mcg every 8hAmerican thyroid association-T4+T3

Monitor thyroid hormone levels every 1-2 daysSupportive careHypothermia –passive rewarming

Hypotension-T4, cautious IV saline, vasopressors(ischemia, arrhythmias)

Hyponatremia –saline, free water restriction

Hypoglycemia –IV dextrose

Bradycardia –monitor, treat arrhythmia (atropine)

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PITUITARY APOPLEXY(sudden attack, struck down)

PRECIPITATING FACTORSPregnancy/delivery(Sheehan’s)Hypertension/hypotension AngiographyDrugs-dopamine agonistsAnticoagulantsDynamic Pituitary function testsMajor surgery-orthopedic surgery, cardiac surgeryVery rareIncidence 1%-26% in P adenomaPotentially lethalAbrupt hemorrhage /infarction of pituitary adenoma-predisposing factor

Hypotension from spinal anaesthesia also may cause pituitary apoplexy-PDPH with visual defects M. LENNON, P. SEIGNE AND A. J. CUNNINGHAM ;BJA 1998,81 616-618

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PITUITARY APOPLEXY

DIFFERENTIAL DIAGNOSISSubarachnoid hemorrhageBacterial meningitisCavernous sinus thrombosis

Midbrain infarctionSymptomIncidenceHeadache95%Vomiting

70%Vision Defects

Visual field defect64%Decreased visual acuity

52%

Diplopia (CN III, IV, V and VI)

78%

Hemiplegia

Rare

Meningismus

Rare

Hypotension (cardiovascular collapse)

95%

CLINICAL FEATURES

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PITUITARY APOPLEXYUSEFUL TESTS IN THE DIAGNOSIS

TESTExpected Result in ApoplexyMRI pituitary Hemorrhagic infarct

ElectrolytesHyponatremiaCBCAnemia, thrombocytopeniaProthrombin time

Possibly prolongedFT4/TSH

Low/Low or normalProlactin

(< 1 ng/dl)

Cortisol, random

Usually < 5 ug/dl

Visual Field

Defects

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PITUITARY APOPLEXYSpontaneous recovery occurs in majority .

Conservative management -preferredDraw blood sample for serum cortisol levels Corticosteroid Hydrocortisone 100-200mg bolus followed by 50-100mg/6h IV/IMIV fluids -5%D & normal salineSurgery -Transsphenoidal surgical decompressionHormonal supplementation

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SUMMARYEndocrine emergensies are potentially life threatening.Delay in diagnosis and treatment can further contribute to high mortality rate associated with these conditions

Diabetic emergencies are relatively common Perioperative management in the operating room for emergency surgeries warrants proper understanding of the pathophysiology and treatment protocols by Anaesthesiologists. Exaggerated stress response

High index of suspicion, early diagnosis and prompt management are essential but challenging.

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