Non diabetic endocrinal emergency

NON DIABETIC NON DIABETIC ENDOCRINAL EMERGENCYENDOCRINAL EMERGENCY

DR JAYANTA DR JAYANTA PAULPAUL

22NDND YEAR PGT YEAR PGT MEDICINE DEPT MEDICINE DEPT

BMCHBMCH

DR JAYANTA DR JAYANTA PAULPAUL

22NDND YEAR PGT YEAR PGT MEDICINE DEPT MEDICINE DEPT

BMCHBMCH

THYROID EMERGENCYTHYROID EMERGENCY

WHAT ARE THOSE WHAT ARE THOSE

THYROID STOMTHYROID STOM MYXEDEMA MYXEDEMA COMACOMA

ACCELERATED HYPERTHYROIDISM ACCELERATED HYPERTHYROIDISM OR OR THYROID STORMTHYROID STORM IS AN EXTREME IS AN EXTREME ACCENTUATION OF THYROTOXICOSISACCENTUATION OF THYROTOXICOSIS

Thyroid stomThyroid stom

It is an uncommon but serious It is an uncommon but serious complication usually occurring in complication usually occurring in association with Graves disease association with Graves disease but sometimes with toxic but sometimes with toxic multinodular goitermultinodular goitercrisis frequently followed thyroidectomy in hyperthyroid patientsThe mortality rate due to cardiac The mortality rate due to cardiac failure arrhythmia or failure arrhythmia or hyperthermia is as high as 30 hyperthermia is as high as 30 even with treatmenteven with treatment

GeneralGeneral Infection Infection

Non-thyroidal trauma or surgery Non-thyroidal trauma or surgery Psychosis PsychosisParturitionParturition

Myocardial infarction or other acute Myocardial infarction or other acute medical problemsmedical problemsThyroid specificThyroid specific

Radioiodine Radioiodine High doses of iodine-containing High doses of iodine-containing

compounds (forcompounds (forexample radiographic contrast media)example radiographic contrast media)

Discontinuation of antithyroid drug Discontinuation of antithyroid drug treatmenttreatment

Thyroid injury (palpation infarction of an Thyroid injury (palpation infarction of an adenoma)adenoma)

New institution of amiodarone therapy New institution of amiodarone therapy

Precipitating Precipitating factorsfactors in thyroid in thyroid stormstorm

DELIRIUM DELIRIUM

SEVERE SEVERE TACHYCARDIATACHYCARDIA

VOMITING VOMITING

DIARRHEA DIARRHEA

DEHYDRATIONDEHYDRATION

IN MANY CASES IN MANY CASES VERY HIGH FEVERVERY HIGH FEVER

Clinical featuresClinical features

Thyrotoxic crisis is usually of abrupt onset and occurs in Thyrotoxic crisis is usually of abrupt onset and occurs in patients in whom preexisting thyrotoxicosis has been patients in whom preexisting thyrotoxicosis has been treated incompletely or has not been treated at alltreated incompletely or has not been treated at all

RELATED TO CYTOKINE RELEASE RELATED TO CYTOKINE RELEASE AND AND

ACUTE IMMUNOLOGIC DISTURBANCE ACUTE IMMUNOLOGIC DISTURBANCE CAUSED BY THE PRECIPITATING CAUSED BY THE PRECIPITATING

CONDITION CONDITION

THE SERUM THYROID HORMONE THE SERUM THYROID HORMONE LEVELS IN CRISIS ARE NOT LEVELS IN CRISIS ARE NOT

APPRECIABLY GREATER THAN THOSE IN APPRECIABLY GREATER THAN THOSE IN SEVERE UNCOMPLICATED SEVERE UNCOMPLICATED

THYROTOXICOSIS BUT THYROTOXICOSIS BUT THE PATIENT THE PATIENT CAN NO LONGER ADAPT TO THE CAN NO LONGER ADAPT TO THE

METABOLIC STRESSMETABOLIC STRESS

The mechanism by which The mechanism by which such factors such factors worsen worsen thyrotoxicosis thyrotoxicosis

1048708 1048708 NOTE THAT FINDINGS ARE NOT DIFFERENT THAN NOTE THAT FINDINGS ARE NOT DIFFERENT THAN THAT OFTHAT OF

HYPERTHYROIDISM BUT THE DIFFERENCE IS IN HYPERTHYROIDISM BUT THE DIFFERENCE IS IN THETHE

SETTING KEY IS FEVER (TYPICALLY gt 40 C 104 F)SETTING KEY IS FEVER (TYPICALLY gt 40 C 104 F)

1048708 1048708 YOU CAN BE ADMITTED WITH HYPERTHYROIDISM YOU CAN BE ADMITTED WITH HYPERTHYROIDISM THATTHAT

IS SEVERE YET IS NOT THYROID STORM IS SEVERE YET IS NOT THYROID STORM (HYPERTHYROID(HYPERTHYROID

TACHYARRHYTHMIAS ARE SERIOUS BUT NOT TACHYARRHYTHMIAS ARE SERIOUS BUT NOT ldquoSTORMrdquo)ldquoSTORMrdquo)

1048708 1048708 THYROID HORMONE LEVELS ARE NOT MUCH THYROID HORMONE LEVELS ARE NOT MUCH DIFFERENTDIFFERENT

IN STORMING THAN IN OTHER CASES SO LIKELY IN STORMING THAN IN OTHER CASES SO LIKELY OTHEROTHER

PREDISPOSING FACTORS (STRESS METABOLIC PREDISPOSING FACTORS (STRESS METABOLIC FACTORS)FACTORS)

Hyperthyroid Hyperthyroid vsvs Thyroid Thyroid StormStorm

MAJOR PART MAJOR PART IS SUPPORTIVE CARE WITH IS SUPPORTIVE CARE WITH HYDRATION COOLING BLANKETS AND HYDRATION COOLING BLANKETS AND ANTIPYRETICS (ACETAMINOPHENANTIPYRETICS (ACETAMINOPHEN))

managementmanagement

1048708 1048708 Avoid aspirin (case reports that it Avoid aspirin (case reports that it releases thyroid hormone from its releases thyroid hormone from its binding globulin worsens case)binding globulin worsens case)

1048708 1048708 Intensive therapy with anti-thyroid Intensive therapy with anti-thyroid drugs beta-blockers steroids iodine drugs beta-blockers steroids iodine solutionssolutions

PROPYLTHIOURACILPROPYLTHIOURACIL WHICH INHIBITS THYROID WHICH INHIBITS THYROID HORMONE SYNTHESIS HORMONE SYNTHESIS AND AND CONVERSION OF CONVERSION OF THYROXINE TO TRI IODOTHYRONINE THYROXINE TO TRI IODOTHYRONINE IS GIVEN BY IS GIVEN BY MOUTH NASOGASTRIC TUBE OR RECTALLY AT A MOUTH NASOGASTRIC TUBE OR RECTALLY AT A RATE OF 300 TO 400 MG EVERY 4ndash6 HOURSRATE OF 300 TO 400 MG EVERY 4ndash6 HOURS

Anti-thyroid drugsAnti-thyroid drugs

Carbimazole is less useful since Carbimazole is less useful since it does not it does not inhibit conversion of thyroxine to tri-inhibit conversion of thyroxine to tri-iodothyronineiodothyronineOne hour after starting propylthiouracil One hour after starting propylthiouracil iodide (iodide (for example eight drops of Lugolrsquos for example eight drops of Lugolrsquos iodine every six hoursiodine every six hours) is given to inhibit ) is given to inhibit thyroidthyroidhormone releasehormone releaseAlternatively if available the radiographic Alternatively if available the radiographic contrast media sodium ipodate or iopanoic contrast media sodium ipodate or iopanoic acid can be given orally with a loading dose acid can be given orally with a loading dose of 2 g followed by 1 g daily These agents also of 2 g followed by 1 g daily These agents also inhibit conversion of thyroxine to tri-inhibit conversion of thyroxine to tri-iodothyronineiodothyronine

Theoretically propylthiouracil should be Theoretically propylthiouracil should be administered before iodine to inhibit the administered before iodine to inhibit the synthesis of additional thyroid hormone from synthesis of additional thyroid hormone from the administered iodide the administered iodide

Nonetheless because iodide is the only agent Nonetheless because iodide is the only agent that will block release of preformed thyroid that will block release of preformed thyroid hormones from the thyroid gland hormones from the thyroid gland

and and

it blocks its own organification through the it blocks its own organification through the Wolff-Chaikoff effect its administration should Wolff-Chaikoff effect its administration should not be delayed or omitted in the severely toxic not be delayed or omitted in the severely toxic patient if propylthiouracil (or methimazole) is patient if propylthiouracil (or methimazole) is not immediately availablenot immediately available

Beta-blockadeBeta-blockade

High doses of b-blocker should be given High doses of b-blocker should be given and propranolol at and propranolol at

a dose of 80ndash120 mg a dose of 80ndash120 mg every six hoursevery six hours is is recommended High recommended High

output thyrotoxic cardiac failure will output thyrotoxic cardiac failure will respond to control of the respond to control of the

heart rate and therefore b-blockade heart rate and therefore b-blockade should be used (with should be used (with

caution) while in general the response to caution) while in general the response to digoxin and digoxin and

diuretics is poordiuretics is poor

In the absence of cardiac insufficiency or In the absence of cardiac insufficiency or asthma a β-adrenergic blocking agent should asthma a β-adrenergic blocking agent should be given to ameliorate the hyperadrenergic be given to ameliorate the hyperadrenergic statestate

If β-adrenergic blocking agents are If β-adrenergic blocking agents are contraindicated a calcium channel contraindicated a calcium channel blocker (diltiazem) may be used to slow blocker (diltiazem) may be used to slow the heart ratethe heart rate

a very short-acting β-adrenergic blocker a very short-acting β-adrenergic blocker such as labetalol or esmolol may be such as labetalol or esmolol may be safer than propranolol in this situationsafer than propranolol in this situation

High-output congestive heart failure High-output congestive heart failure can develop in patients with severe can develop in patients with severe thyrotoxicosis and a β-adrenergic thyrotoxicosis and a β-adrenergic antagonist may further reduce cardiac antagonist may further reduce cardiac output output

SteroidsSteroids

Large doses of dexamethasone (8 mg Large doses of dexamethasone (8 mg orally once daily) should be given to orally once daily) should be given to support the response to stress inhibit support the response to stress inhibit both the release of hormone from the both the release of hormone from the gland and the peripheral generation of Tgland and the peripheral generation of T33 from Tfrom T44 synergizing with iodide and synergizing with iodide and propylthiouracil respectively in these propylthiouracil respectively in these actionsactions The combined use of propylthiouracil The combined use of propylthiouracil iodide and dexamethasone can restore iodide and dexamethasone can restore the concentration of Tthe concentration of T33 to normal within to normal within 24 to 48 hours24 to 48 hours

Cholestyramine 4 g every 6ndash8 hours Cholestyramine 4 g every 6ndash8 hours bindsbindsthyroid hormone in the gut and thus thyroid hormone in the gut and thus interrupts the modestinterrupts the modestenterohepatic circulation of thyroid enterohepatic circulation of thyroid hormone its use will lead to a more hormone its use will lead to a more rapid lowering of circulating thyroid rapid lowering of circulating thyroid hormoneshormones

CholestyramineCholestyramine

Supportive measures Supportive measures

correction of dehydration and correction of dehydration and hypernatremia if present and hypernatremia if present and administration of glucoseadministration of glucoseHyperpyrexia should be treated Hyperpyrexia should be treated vigorouslyvigorouslyIn mild cases acetaminophen may In mild cases acetaminophen may suffice but a cold blanket or ice packs suffice but a cold blanket or ice packs may be required may be required Salicylates should be avoided because Salicylates should be avoided because they compete with Tthey compete with T33 and T and T44 for for binding to TBG and transthyretin (TTR) binding to TBG and transthyretin (TTR) and therefore increase the free and therefore increase the free hormone levelshormone levelsIn addition high doses of salicylates In addition high doses of salicylates increase the metabolic rateincrease the metabolic rate

If heart failure or pulmonary congestion If heart failure or pulmonary congestion is present appropriate diuretics are is present appropriate diuretics are indicated indicated

In patients with atrial fibrillation the In patients with atrial fibrillation the rapid ventricular response requires rapid ventricular response requires appropriate blockade of atrioventricular appropriate blockade of atrioventricular node conductionnode conduction

When treatment is successfulWhen treatment is successful improvement improvement is usually manifested within is usually manifested within 1 or 2 days and 1 or 2 days and recovery recovery occurs within a occurs within a week At this time iodide and week At this time iodide and dexamethasone can be withdrawn and dexamethasone can be withdrawn and plans for long-term management are plans for long-term management are mademade

Follow upFollow up

After implementation of this four-pronged approach to management of thyrotoxic storm dramatic clinical improvement is usually seen within 12 to 24 hours in most patients who survive

Myxedema comaMyxedema coma

Myxedema coma is a severe life-Myxedema coma is a severe life-threatening sequela of profound threatening sequela of profound hypothyroidismhypothyroidism Myxedema coma is the Myxedema coma is the ultimate stage of severe longstanding ultimate stage of severe longstanding hypothyroidismhypothyroidismSevere hypothyroidism with metabolic Severe hypothyroidism with metabolic shutdown (cardiac hepatic other shutdown (cardiac hepatic other organs)organs)This state which almost invariably This state which almost invariably affects older patients occurs most affects older patients occurs most commonly during the winter months and commonly during the winter months and is associated with a high mortality rateis associated with a high mortality rateVery high mortality 13Very high mortality 13

Typical patientTypical patient elderly female with elderly female with longstandinglongstandinghypothyroidismhypothyroidism

Precipitating factorsPrecipitating factors Exacerbating factorsExacerbating factors

Hypothermia Hypothermia

Infection Infection

Cerebrovascular Cerebrovascular accident accident

DrugsDrugs Anesthetics Anesthetics

Tranquilizers Tranquilizers Amiodarone Amiodarone Sedatives Sedatives Narcotics Narcotics

Trauma Trauma

Gastrointestinal bleedingGastrointestinal bleeding

HypoglycemiaHypoglycemia

Hyponatremia Hyponatremia

Hypoxemia Hypoxemia

Hypercapnia Hypercapnia

Acidosis Acidosis

HypercalcemiaHypercalcemia

Precipitating Precipitating factorsfactors in myxoedema coma in myxoedema coma


The three main features are The three main features are Altered mental state ranging from poor Altered mental state ranging from poor cognitive function through psychosis to cognitive function through psychosis to comacoma

Hypothermia (as low as 23˚C) or absence Hypothermia (as low as 23˚C) or absence of fever in spite of severe infection of fever in spite of severe infection (prognosis worsens as the core(prognosis worsens as the coreTemperature fall) Temperature fall)

The presence of a precipitating eventThe presence of a precipitating event

Hallmark signs of hypothyroidism will be Hallmark signs of hypothyroidism will be presentmdashpresentmdashdry coarse scaly skin sparse dry coarse scaly skin sparse or coarse hair nonpitting edema of the or coarse hair nonpitting edema of the periorbital regions hands and feet periorbital regions hands and feet macroglossia hoarseness and delayed macroglossia hoarseness and delayed deep tendon reflexesdeep tendon reflexes

cns manifestations cns manifestations

The patient may have a history of using a The patient may have a history of using a CNS depressant narcotic or sedative CNS depressant narcotic or sedative

About 25 of patients with myxedema coma About 25 of patients with myxedema coma have focal or generalized seizureshave focal or generalized seizures

Severe sensorial depression helliphellipcomaSevere sensorial depression helliphellipcoma

CARDIAC CARDIAC MANIFESTATION MANIFESTATION

Although frank heart failure is rare Although frank heart failure is rare cardiomegaly bradycardia and decreased cardiomegaly bradycardia and decreased cardiac contractility are common features of cardiac contractility are common features of cardiovascular involvement in myxedema cardiovascular involvement in myxedema coma coma Cardiac enlargement (Cardiac enlargement (myxedema heartmyxedema heart) is ) is often due tooften due topericardial effusion pericardial effusion

GI tract manifestation GI tract manifestation

astrointestinal tract involvement in astrointestinal tract involvement in myxedema coma may result in decreased myxedema coma may result in decreased intestinal motility paralytic ileus or intestinal motility paralytic ileus or megacolon causing patients to present with megacolon causing patients to present with abdominal pain constipation and nauseaabdominal pain constipation and nauseaOral medications may be ineffective because Oral medications may be ineffective because of these problems of these problems Renal manifestation Renal manifestation

Hyponatremia and decreased glomerular Hyponatremia and decreased glomerular filtration rate occurfiltration rate occurthe kidneys lose their ability to excrete a the kidneys lose their ability to excrete a water load because of decreased delivery of water load because of decreased delivery of water to the distal nephron as well as water to the distal nephron as well as increased production of antidiuretic increased production of antidiuretic hormonehormone

Biochemical abnormalitiesBiochemical abnormalities

hyponatraemia normal or increased hyponatraemia normal or increased urine sodium excretionurine sodium excretion

raised creatine phosphokinase and raised creatine phosphokinase and lactate dehydrogenase hypoglycaemialactate dehydrogenase hypoglycaemia

normocytic or macrocytic anaemianormocytic or macrocytic anaemia

Thyroid stimulating hormone values may Thyroid stimulating hormone values may only bemodestly raised (and will be only bemodestly raised (and will be normal or low in secondary normal or low in secondary hypothyroidism) but free thyroxine hypothyroidism) but free thyroxine levels are usually very lowlevels are usually very low

Three major etiologiesThree major etiologies

1048708 1048708 Undiagnosed hypothyroidism Undiagnosed hypothyroidism (autoimmune(autoimmunethyroiditis radiation hypothyroidism thyroiditis radiation hypothyroidism etc)etc)

1048708 1048708 More commonly discontinuation of More commonly discontinuation of therapy ortherapy orrunning out of medication (for months)running out of medication (for months)

1048708 1048708 Iatrogenic stopping patients for I-131 Iatrogenic stopping patients for I-131 cancer Rxcancer Rx

MANAGEMENTMANAGEMENT

The importance of the difficulty in The importance of the difficulty in diagnosing myxedema coma is that a diagnosing myxedema coma is that a delay in therapy worsens the prognosisdelay in therapy worsens the prognosisConsequently the diagnosis should be Consequently the diagnosis should be made on clinical grounds and after made on clinical grounds and after sending serum for thyroid function tests sending serum for thyroid function tests therapy should be initiated without therapy should be initiated without awaiting the results of confirmatory awaiting the results of confirmatory tests tests because mortality may be 20 or because mortality may be 20 or higherhigherEven with prompt recognition and Even with prompt recognition and treatment mortality istreatment mortality is20ndash3020ndash30

The three principles of management are The three principles of management are

1 Rapid institution of thyroid hormone 1 Rapid institution of thyroid hormone replacement replacement

2 Treatment of the precipitating cause 2 Treatment of the precipitating cause andand

3 provision of ventilatory and other 3 provision of ventilatory and other supportsupport

lsquolsquolsquolsquoHigh dosersquorsquo regimens may be given as High dosersquorsquo regimens may be given as followsfollows ififintravenous thyroxine is available this intravenous thyroxine is available this can be given as acan be given as abolus of 300ndash500 mg followed by 50ndash100 bolus of 300ndash500 mg followed by 50ndash100 mg daily mg daily

Oral thyroxine in similar doses can be Oral thyroxine in similar doses can be given (usually bygiven (usually bynasogastric tube) but absorption may nasogastric tube) but absorption may be impairedbe impaired

thyroid hormone replacementthyroid hormone replacement

There is a theoretical concern There is a theoretical concern thatthat conversion of thyroxine to conversion of thyroxine to triiodothyronine will be impaired triiodothyronine will be impaired due todue to the effects of any illness on deiodinase the effects of any illness on deiodinase activity and therefore the use of activity and therefore the use of triiodothyronine instead of thyroxine has triiodothyronine instead of thyroxine has been advocated been advocated but this also has the but this also has the potential to cause adverse cardiac potential to cause adverse cardiac effects when given too rapidlyeffects when given too rapidly The usual intravenous dose of The usual intravenous dose of triiodothyronine is 10ndash20 mg initially triiodothyronine is 10ndash20 mg initially followed by followed by 10 mg every four hours for 10 mg every four hours for 24 hours 24 hours thenthen 10 mg every six hours 10 mg every six hours Oral treatment with similar doses is also Oral treatment with similar doses is also possiblepossible A further variation is to give A further variation is to give 200 200 mg thyroxine with 10 mg mg thyroxine with 10 mg triiodothyronine initially and triiodothyronine initially and thenthen tri- tri-iodothyronine 10 mg every 12 hours and iodothyronine 10 mg every 12 hours and thyroxine 100 mg every 24 hours thyroxine 100 mg every 24 hours until until the patient resumes normal thyroxine the patient resumes normal thyroxine orallyorally

The authors recommend ECG The authors recommend ECG monitoring and carefulmonitoring and carefultitration of thyroid replacement therapy titration of thyroid replacement therapy against any definiteagainst any definiteischaemic ECG abnormalitiesischaemic ECG abnormalitiessteroidsteroid

Hydrocortisone (5 to 10 mghr) should Hydrocortisone (5 to 10 mghr) should also be given because of the possibility also be given because of the possibility of relative adrenocortical insufficiency as of relative adrenocortical insufficiency as the metabolic rate increasesthe metabolic rate increasesANTIBIOTICSANTIBIOTICS

Treatment of the underlying Treatment of the underlying precipitant is usually straightforward precipitant is usually straightforward Broad spectrum antibiotics should be Broad spectrum antibiotics should be considered if there is no obvious cause considered if there is no obvious cause as the signs of an infection may be as the signs of an infection may be obscure yet this is the underlying cause obscure yet this is the underlying cause in up to a third of casesin up to a third of cases

OTHEROTHERSS

A critical element in therapy is A critical element in therapy is support of respiratory function by means support of respiratory function by means of assisted ventilation and controlled of assisted ventilation and controlled oxygen administrationoxygen administration All patients should be admitted to All patients should be admitted to intensive care or theintensive care or theHDU most patients require ventilatory HDU most patients require ventilatory support for 1ndash2 dayssupport for 1ndash2 days Hypothermia should be treated with Hypothermia should be treated with space blankets since active external space blankets since active external rewarming leads to circulatory collapse rewarming leads to circulatory collapse due to peripheral vesodilatationdue to peripheral vesodilatation Cautious volume expansion using Cautious volume expansion using intravenous saline usually suffices but intravenous saline usually suffices but hypertonic saline may need to be hypertonic saline may need to be considered if the serum sodium is very considered if the serum sodium is very low (120 mmoll)low (120 mmoll)

Intravenous glucose may be required for Intravenous glucose may be required for hypoglycaemiahypoglycaemia

General measures applicable to the General measures applicable to the comatose patient should be undertaken comatose patient should be undertaken such as frequent turning prevention of such as frequent turning prevention of aspiration and attention to fecal aspiration and attention to fecal impaction and urinary retentionimpaction and urinary retention

Finally the physician should assess Finally the physician should assess the patient for the presence of the patient for the presence of coexisting disease such as infection and coexisting disease such as infection and cardiac or cerebrovascular disease cardiac or cerebrovascular disease In particular the myxedematous In particular the myxedematous patient may be afebrile despite a patient may be afebrile despite a significant infection As soon as the significant infection As soon as the patient is able to take medication by patient is able to take medication by mouth treatment with oral mouth treatment with oral levothyroxine should be institutedlevothyroxine should be instituted

Pituitary emergencyPituitary emergency

Pituitary apoplexy is caused by Pituitary apoplexy is caused by haemorrhagic infarction of a pituitary haemorrhagic infarction of a pituitary tumour or less commonly the normal tumour or less commonly the normal pituitary glandpituitary gland

Acute pituitary apoplexyAcute pituitary apoplexy

This may cause volume expansion with This may cause volume expansion with local mass effectlocal mass effect Apoplexy is an endocrine Apoplexy is an endocrine emergency that emergency that may result in severe may result in severe hypoglycemia hypotension central hypoglycemia hypotension central nervous system (CNS) hemorrhage and nervous system (CNS) hemorrhage and death death Prompt recognition is needed to Prompt recognition is needed to prevent cardiovascular collapse prevent cardiovascular collapse secondary to pituitary-adrenal secondary to pituitary-adrenal hypofunction There is an equal sex hypofunction There is an equal sex incidenceincidence

Pituitary apoplexy may occurPituitary apoplexy may occur spontaneously in a preexisting adenoma spontaneously in a preexisting adenoma post-partum (Sheehans syndrome) or in post-partum (Sheehans syndrome) or in association with diabetes hypertension association with diabetes hypertension sickle cell anemia or acute shocksickle cell anemia or acute shock The hyperplastic enlargement of The hyperplastic enlargement of the pituitary during pregnancy increases the pituitary during pregnancy increases the risk for hemorrhage andinfarction the risk for hemorrhage andinfarction


These resemble those of subarachnoid These resemble those of subarachnoid haemorrhagehaemorrhage

severe headache nausea (80) severe headache nausea (80) vomiting (60) photophobia(50) and vomiting (60) photophobia(50) and loss of consciousness (10) loss of consciousness (10)

Neuro-ophthalmic signs include Neuro-ophthalmic signs include

ocular paresis in up to 70 of cases with ocular paresis in up to 70 of cases with IIIrd (67) IVth (4) and Vth (29) IIIrd (67) IVth (4) and Vth (29) nerve palsies nerve palsies Visual field defects and even blindness Visual field defects and even blindness

Pre-existing endocrine dysfunctionPre-existing endocrine dysfunction is present is present in 20ndash30 in 20ndash30

patient may have circulatory collapsepatient may have circulatory collapse

Management Management

If pituitary apoplexy is suspected If pituitary apoplexy is suspected (or confirmed by urgent magnetic (or confirmed by urgent magnetic resonance imaging or computed resonance imaging or computed tomography) hydrocortisone 100 mg tomography) hydrocortisone 100 mg intramuscularly six hourly or 4 mg hour intramuscularly six hourly or 4 mg hour intravenously should beadministered intravenously should beadministered without delay and continued until the without delay and continued until the crisis is overcrisis is over Those with significant or progressive Those with significant or progressive visual loss or loss of consciousness visual loss or loss of consciousness require urgent surgical decompressionrequire urgent surgical decompression

Visual recovery after surgery is Visual recovery after surgery is inversely correlated with the length of inversely correlated with the length of time after the acute eventtime after the acute eventTherefore severe ophthalmoplegia or Therefore severe ophthalmoplegia or visual deficits are indications for early visual deficits are indications for early surgerysurgery

Early neurosurgical intervention is Early neurosurgical intervention is associated with improved neuro-associated with improved neuro-ophthalmic outcome with reported ophthalmic outcome with reported improvements in visual acuity and fields improvements in visual acuity and fields of 86 andof 86 and76 respectively76 respectively

Acute Adrenal InsufficiencyAcute Adrenal Insufficiency

11 Following Stress (trauma surgery Following Stress (trauma surgery infection or prolonged fasting) in patient infection or prolonged fasting) in patient with latent insufficiencywith latent insufficiency

2 2 Following sudden withdrawal of Following sudden withdrawal of adrenocortical hormone in a patient with adrenocortical hormone in a patient with chronic insufficiencychronic insufficiency

33 Following bilateral adrenalectomy or a Following bilateral adrenalectomy or a functioning adrenal tumor that had functioning adrenal tumor that had suppressed the other adrenalsuppressed the other adrenal

44 Following sudden destruction of the Following sudden destruction of the pituitary gland (pituitary necrosis) or pituitary gland (pituitary necrosis) or when thyroid hormone is given to a pt when thyroid hormone is given to a pt with hypoadrenalismwith hypoadrenalism

55 Following injury to both adrenals by Following injury to both adrenals by trauma hemorrhage anticoagulant trauma hemorrhage anticoagulant therapy thrombosis infection or therapy thrombosis infection or metastatic carcinomametastatic carcinoma

Cooper MS Stewart PM Corticosteroid insufficiency in Cooper MS Stewart PM Corticosteroid insufficiency in acutely ill patients N Engl J Med 2003348727-734acutely ill patients N Engl J Med 2003348727-734

Causes Causes

Dehydration hypotension or shock out of Dehydration hypotension or shock out of proportion to severity of current illnessproportion to severity of current illness

Nausea and vomiting with a history of weight lost Nausea and vomiting with a history of weight lost and anorexia and anorexia Abdominal pain so-called acute abdomen Abdominal pain so-called acute abdomen

Unexplained hypoglycemia Unexplained hypoglycemia

Unexplained fever Unexplained fever

CLINICAL AND LABORATORY FEATURES OF CLINICAL AND LABORATORY FEATURES OF AN ADRENAL CRISISAN ADRENAL CRISIS

Hyponatremia hyperkalemia azotemia Hyponatremia hyperkalemia azotemia hypercalcemia or eosinophilia hypercalcemia or eosinophilia Hyperpigmentation or vitiligo

Other autoimmune endocrine deficiencies such Other autoimmune endocrine deficiencies such as hypothyroidism or gonadal failureas hypothyroidism or gonadal failure

Adrenal Insufficiency Adrenal Insufficiency DiagnosisDiagnosis

Rapid ACTH Stimulation TestRapid ACTH Stimulation Test

Not influenced by diurnal variations in Not influenced by diurnal variations in cortisol secretioncortisol secretion

Baseline cortisol sample ACTH Baseline cortisol sample ACTH 250mcg Post-ACTH plasma cortisol at 250mcg Post-ACTH plasma cortisol at 30min and 60min p injection30min and 60min p injection

Baseline above 34 is normal and less Baseline above 34 is normal and less than 15 is evidence of insufficiency than 15 is evidence of insufficiency When between the two the incriment When between the two the incriment increase with ACTH should be greater increase with ACTH should be greater than 9mcgdLthan 9mcgdL

TREATMENT OF ACUTE TREATMENT OF ACUTE ADRENAL INSUFFICIENCY ADRENAL INSUFFICIENCY (ADRENAL CRISIS)(ADRENAL CRISIS)

EMERGENCY MEASUREEMERGENCY MEASURE

11

Establish intravenous access with a large-Establish intravenous access with a large-gauge needle gauge needle

22

Draw blood for stat serum electrolytes and Draw blood for stat serum electrolytes and glucose and routine measurement of plasma glucose and routine measurement of plasma cortisol and ACTH Do not wait for laboratory cortisol and ACTH Do not wait for laboratory results results

33

Infuse 2 to 3 L of 154 mmolL NaCl (09 Infuse 2 to 3 L of 154 mmolL NaCl (09 saline) solution or 50 gL (5) dextrose in 154 saline) solution or 50 gL (5) dextrose in 154 mmolL NaCl (09 saline) solution as quickly mmolL NaCl (09 saline) solution as quickly as possible Monitor for signs of fluid overload as possible Monitor for signs of fluid overload by measuring central or peripheral venous by measuring central or peripheral venous pressure and listening for pulmonary rales pressure and listening for pulmonary rales Reduce infusion rate if indicated Reduce infusion rate if indicated

44

Inject intravenous hydrocortisone (100 mg Inject intravenous hydrocortisone (100 mg immediately and every 6 hr) immediately and every 6 hr)

55

Use supportive measures as needed Use supportive measures as needed

SUBACUTE MEASURES AFTER SUBACUTE MEASURES AFTER STABILIZATION OF THE PATIENSTABILIZATION OF THE PATIEN

1 1 Continue intravenous 154 Continue intravenous 154 mmolL NaCl (09 saline) mmolL NaCl (09 saline) solution at a slower rate for solution at a slower rate for next 24 to 48 hr next 24 to 48 hr

2 2 Search for and treat possible Search for and treat possible infectious precipitating causes infectious precipitating causes of the adrenal crisis of the adrenal crisis

3 3 Perform a short ACTH Perform a short ACTH stimulation test to confirm the stimulation test to confirm the diagnosis of adrenal diagnosis of adrenal insufficiency if patient does not insufficiency if patient does not have known adrenal have known adrenal insufficiency insufficiency

4 4 Determine the type of adrenal Determine the type of adrenal insufficiency and its cause if not insufficiency and its cause if not already known already known

5 5 Taper glucocorticoids to Taper glucocorticoids to maintenance dosage over 1 to 3 maintenance dosage over 1 to 3 days if precipitating or days if precipitating or complicating illness permits complicating illness permits

6 6 Begin mineralocorticoid Begin mineralocorticoid replacement with replacement with fludrocortisone (01 mg by fludrocortisone (01 mg by mouth daily) when saline mouth daily) when saline infusion is stopped infusion is stopped

Thank you

Thank you

THYROID EMERGENCYTHYROID EMERGENCY















DELIRIUM DELIRIUM


VOMITING VOMITING

DIARRHEA DIARRHEA







CONDITION CONDITION

























and and













SteroidsSteroids









Follow upFollow up







Infection Infection




Trauma Trauma




Hypoxemia Hypoxemia


Acidosis Acidosis







































OTHEROTHERSS




























Causes Causes















11


22


33


44


55









Thank you

Thank you















DELIRIUM DELIRIUM


VOMITING VOMITING

DIARRHEA DIARRHEA







CONDITION CONDITION

























and and













SteroidsSteroids









Follow upFollow up







Infection Infection




Trauma Trauma




Hypoxemia Hypoxemia


Acidosis Acidosis







































OTHEROTHERSS




























Causes Causes















11


22


33


44


55









Thank you

Thank you



CONDITION CONDITION

























and and













SteroidsSteroids









Follow upFollow up







Infection Infection




Trauma Trauma




Hypoxemia Hypoxemia


Acidosis Acidosis







































OTHEROTHERSS




























Causes Causes















11


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33


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and and













SteroidsSteroids









Follow upFollow up







Infection Infection




Trauma Trauma




Hypoxemia Hypoxemia


Acidosis Acidosis







































OTHEROTHERSS




























Causes Causes















11


22


33


44


55









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SteroidsSteroids









Follow upFollow up







Infection Infection




Trauma Trauma




Hypoxemia Hypoxemia


Acidosis Acidosis







































OTHEROTHERSS




























Causes Causes















11


22


33


44


55









Thank you

Thank you








Follow upFollow up







Infection Infection




Trauma Trauma




Hypoxemia Hypoxemia


Acidosis Acidosis







































OTHEROTHERSS




























Causes Causes















11


22


33


44


55









Thank you

Thank you






Infection Infection




Trauma Trauma




Hypoxemia Hypoxemia


Acidosis Acidosis







































OTHEROTHERSS




























Causes Causes















11


22


33


44


55









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Thank you





































OTHEROTHERSS




























Causes Causes















11


22


33


44


55









Thank you

Thank you



























Causes Causes















11


22


33


44


55









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Thank you















11


22


33


44


55









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Thank you








Thank you

Thank you

Non diabetic endocrinal emergency

Health & Medicine

Transcript of Non diabetic endocrinal emergency