Non-Diabetic Emergencies – EMERGENCY LECTURE

by birtanpublished on August 5, 2020

welcome guys non-diabetic emergencies so why non-diabetic these are uncommon but potentially lethal the main basis of this is um

Hypothalamic pituitary axis so now the hypothalamus releases the corticotropin release factor of the release hormone which acts on the pituitary to release acthr the adrenal corticotrophic hormone

Which acts on the adrenal glands to really release cortisol and endosterone now these non-diabetic emergencies are uncommon but they're lethal they are very difficult to diagnose an

Ed treatment may be life-saving so let's have a look about a bit of a background thyroid and thyroid related emergencies like stomach cellular coma

And adrenal crisis what are the main clinical features and what investigations are required and of course what is a treatment for these all right so hyper or hypothyroidism

Original insufficiency usually have non-specific symptoms like fatigue weakness and depression they're usually difficult to diagnose now the classic manifestations are most

Easily identified with increasing theory acute stresses can precipitate life-threatening events and management is based on the clinical judgment an example is a 45 year old female comes

With tachycardia for two days chest pain breathing difficulty weight loss our appetite is normal very high temperature rapid speech and tremors

Now to help you there's a clinical picture which is possibly classic and characteristic and these are the ecg findings what do you think is happening here so this is hypothyroidism

All right so thyroid toxicosis is defined as any state in which thyroid hormone levels are increased in the blood over production can happen in graves disease toxic multi-nautical glider

Or thymine hormone released from an injured gland like thyroiditis or if you have given exogenous thyroid hormone to common is about point five to two point two percent

More than fifty percent of patients are subclinical pre-hyperthyroid states depress thyroid stimulating hormone and normal free t4 it is prevalent in women tenfold

As compared to men now if you look at the basic science thyroid system it's basically the hypothalamus anti-repatry gland uh thyroid thyrotropin release hormone is released

Which causes release of thyroid stimulating hormone now this thyroid stimulating hormone stimulates the thyroid gland which in turn releases the thyroid hormones d3 and d4 and increases

Metabolism growth and development and increased catecholamine effect if you look at the biosynthesis it's mainly in the follicular cells thyroglobulin is a large hormonal precursor protein

With numerous tyrosines now iodine is actively transported into the follicular cells in iodized and oxidized sorry when bound to tyrosine residues so the iodo tyrosines plus thyroglobulin

From the t4 and t3 which are released into the circulation by proteolysis all t4 produced in the thyroid gland whereas 15 to 20 20 percent of t3 is synthesized directly and remainder is why the iodination of

T4 in peripheral tissues okay so t4 whole of it is producing a thyroid gland d3 only 20 percent is directly synthesized rest is while the iodination of t4 in the

Peripheral tissues if you look at the most common cause of thyroid toxicosis it's a graves disease hypothyroidism diffuse symmetrical goida ophthalmology and dermapathy other

Characteristic features primarily in the female 20 to 40 years and often those with a family history of thyroid disease so autoimmune disorders b lymphocytes produce immunoglobulins that stimulates

The tsh receptor eye disease thought to result from thyroid antibodies sensitized to common antigen in orbital fibroblasts and muscles d3 and d4 increase the number and

Sensitivity of beta adenergic receptors dramatically increasing the response to endogenous catecholamines toxic goiter is the second leading cause of hyperthyroidism multiple autonomous functioning nodules

Women more than 50 are iron deficient iron chicken populations include central africa central america himalayas and europe symptoms are milder than grey's disease

And gradually onset now iodine replacement given to an iodine deficient individual can cause jawed based effect which is acute presentation due to increased substrate

I repeat it again iodine replacement given to an iodine deficient individual can cause a dirt based effect which leads to an acute presentation due to increased substrate

And due to the age atrial fibrillation and congestive heart failure are common tremors and hyper metabolic features are less weird muscle wasting and weakness is common the pathophysiology of thyroid storm

Includes acute stress which leads to surge of catacolamines examples include glycogenolysis and cataclysmin-mediated antagonism of insulin hyperglycemia free t4 and t3 are released to

Catecholamine binding states and heightened response happens to a genetic stimuli so this is a diagnostic criteria for thyroid storm so this is an exaggeration of clinical

Manifestations of thyroid toxicosis which is further distinguished by the presence of fever tachycardia cns dysfunction and gastrointestinal symptoms decompensation of one or more organ

Systems happens as a shock or heart failure patient complaints and thyrotoxicosis are as follows these are variable and involve a multitude of systems so constitution like weight loss

Hyper metabolic like heat intolerance respiratory like tachycardia heat pounding psychiatric like anxiety restlessness muscular tremors tearing irritation sensitivity in the

Eye neck fullness and dysphagia in the thyroid gland you have flushing hair loss and reproductive symptoms like oligomenorrhea decreased libido etc

Etiology undiagnoses were untreated so basically acute precipitation released with higher stone one to two billions percent of patients with thyroid toxicosis will progress into thyroid storm in the

Setting of an acute stressor can lead to 20 mortality causes include craves disease toxic multi-nautical argoida toxic adenoma factitious thyrotoxicosis thyrotoxicosis associated with heart

Attacks hashimoto's subacute postpartum sporadic aminoderon i have been used now these are some of the lesser precipitations of hearthstone you can pause the video here and just go through

Them and just memorize them now disease progression if the underlying hyperthyroidism so there's a weight loss heat intolerance tremors anxiety diarrhea etc

Fever is expected physiological vasodilation for heat dissipation a system is already was alienated due to running heart altered mental status and cosmet mild impairment psychosis and

Frank coma all right so patient population differences all right so the elderly can be difficult to diagnose fever few robot signs of hypothyroidism some of the clues are supraventricular

Tachycardia rhythmia new heart failure the young ones can be difficult to treat the poor toleration of state versus elderly there's a relatively high number of surface beta receptors

Lead exaggerated energy response more likely to die from circulatory collapse then you can also have something called pathetic hyperthyroidism jackal's usually an alibi can be of any age

Correct aside but new onset loss of consciousness atrial fibrillation heart failure angina minimal fever tachycardia no preceding history of hyperthyroidism except weight loss

They're more common than the thyroid storm in these patients to check the thyroid stimulating hormone and basically any patient will use suspected loss of consciousness

Psychiatric presentation atrial fibrillation or congestive heart failure so the investigation that you need to do is a thyroid stimulating hormone and a free t4

But you look at the precipitation and you do a ecg chest x-ray urine labs blood cultures tox screen ct head and maybe a csf if required and the goals of management include decrease in the hormone synthesis on the

Release decrease in the adrenergic symptoms decrease in the peripheral conversion of t4 to t3 and supportive care so decrease of hormonal synthesis is by inhibition of

Thyroid thyroid peroxidase and profile thorough uracil is the drug of choice given 600 1000 milligrams by oral or angioperectyl and then about 250 milligrams

For hourly no iv form pregnancy risk is there's an evidence of fetal harm however it's safe for lactation adverse reactions include rash stephen johnson syndrome

Bone marrow suppression and liver toxicity contraindication therefore include previous hepatic failure or a granulocytosis alternative medications include methymazole

Also not phenotone phenobarbital enhance t4 metabolism second is decrease the hormone release so iodine further decreases release cell storage so given after

One hour after profile thyroid cell iodine load presented to an actively synthesizing gland voids for the substrate for hormone potassium iodide can be given as five

Drops oral ng operectal every six hourly given liu gold solution 8 drops every 6 hourly on lithium 300 milligram every 6 hourly per oral or ng the levels are monitored to maintain a

Level of about one milligram per liter all right so mechanism excess iodide now it inhibits the eyelid trapping and thyroglobulin iodine iodination so this is also called as a wolf chykov effect

Again excess iodine inhibits iodine trapping and thyroglobulin iodination it's called wolf shakov effect it's a autoregulatory phenomenon that inhibits oxidation of iodide in the

Thyroid gland formation of thyroid hormone within the follicle cells and the release of thyroid hormone into the bloodstream it blocks the release of thyroid hormone from the gland

Inhibition of thyroid hormone production and releases transient with the gland escaping inhibition of 10 to 14 days escape phenomenon is believed to occur because of decreased ionogen and inorganic iodine concentration so

Can do down regulation of sodium iodine symporter in the basolateral membrane of the follicular cells now iodide load can induce hyperthyroidism drug based effect in

Some patients with multi-nautical quieter and later graves disease especially in the patient is iodine deficient to begin with all right recover for infection is

Suspected impaired immune response broad spectrum antibiotics for elevated white blood cells symptomatic relief arrhythmia and tachycardia propranolol one milli milligram iv

D half five minutes over ten minutes then 10 to 15 minutes brn is told rated some t4 to t3 plus non-selective effects to improve tachycardia tremor hyperpyrexia and restlessness

Parallel 120 240 milligram if blood pressure is stable otherwise ivf plus observe resupine if beta blocker is contraindicated steroids some inhibition of t4 to t3 conversion can be caused by steroids you

Give hydrocortisone 300 milligram iv then 100 milligrams 6 alley or dexomy thousand two to four milligrams iv6 hourly propyl thyroid uracil and propanol also

Have some effect and treats relative adrenal insufficiency supportive additional care includes fluid rehydration normal saline dextrose 59 normal cell

And depletion of glycogen stores correct the electrolyte abnormalities search for the precipitating congestive heart failure primarily high output beta blockers

Diuretics are not first line given the hypovolemia temperature control so temperature regulations cool missed ice packs and fans acetaminophen asd alt given possible liver compromise

Aspirin is contraindicated because it increases levels of free thyroid hormones risk of aggressive cooling so summary of management includes propylene uracil propranolol

Potassium iodide steroids and supportive care and this is the management of thyroid storm now i'm not going into all these details and you can

Pause the video here and just go through these however pearls in conclusions we should improve overall with an 18 to 24 hours with mental status improvement in a few hours on an average require three to five

Liters of intravenous fluids atrial fibrillation most convert via beta blocker didoxin increase clearance and high dosing is needed calcium channel blockers and

Anticoagulation decrease embolism risk no heart failure now there can be some special situations of thyroid toxicos is a congestive heart failure atrial fibrillation thyroiditis factitious thyrotoxicosis

Okay coming to case two you've got a 36 year old female with history of non-insulin dependent diabetes present to the emergency with altered mental status family reports that she's always cold

Weak and often complains of brittle hair she said to sadly gaining weight despite no change in the food intake and as a productive cough for two weeks with intermittent fever

All right hypothyroidism is prevalence of thyroid stimulating hormone elevations range from 37 to 95 percent with the majority of these having a normal free t4

What hypothyroidism is seen in a minority point three percent of the population overall with the prevalence rising in age so that the patients older than 80 have a fivefold greater likelihood of

Developing hypothyroidism than the 12 to 49 year olds hashimoto's thyroiditis is a thyroid gland failure caused by autoimmune destruction of the gland

Guaita in younger patients is practiced by elevated anti-thyroid antibodies especially to thyroid peroxidase thyroglobulin ntsh tsh receptor antibody in hashimoto's disease

Blocks a receptor in contrast to the stimulating antibody in graves disease end stage graves disease autoimmune destruction of the thyroid gland following severe excavations of hyperthyroidism

Is falling treatment of grace disease with radioactive iodine or thyroidectomy thyroidectomy is not the cause drug induced hypothyroidism can also happen like in iodine excess amidone iodine contrast media key supplements so

Remember the wolf chykov effect that we talked about is an impaired thyroid hormone release and synthesis thereby converting subclinical hypothyroid to avoid hypothyroidism and

Sometimes precipitating hypothyroidism de novo there are many causes for hypothyroidism you can again pause the video here and just go through all the causes to remember

All right so mexico is a decompensated hypothyroidism with vascular collapse so metabolic rate leads to decreased body temperature and vasoconstrictions and decreased metabolic rate decreases decreased body

Temperature and waste of construction on examination a patient appears older than the stated age cool to touch dry skin mild hypertension altered mental state hypothermia there is swelling on the hands face feet

Periorbital tissues accumulation of glycosamine glycogens in interstitial fluids and associated with capillary leak is delete delayed deep 10 relaxation so there's an acute decompensation so

Infection for example leads away dilatation and vascular collapse in hemodynamics there is a reduced cardiac output and blood volume so what is the etiology of mixed animal

Coma it could mean undiagnosed or untreated it could be resulting to hashimoto's thyroiditis or post-surgery so basically there's an acute precipitating which leads to mexicama coma

Some of the precipitants include infection trauma vascular non-compliance with treatment any acute medical illness or cold some of the aggravating or precipitating

Factors are listed here so common ones include infection exposure to cold cerebrovascular accident microlyn infaction etc so recognition so elderly female in the

Winter known hypothyroidism hypothermia altered mental states hypotension slow respiration should indicate towards this condition symptoms and size are listed here again

You can just pause the video and just go through them but the common diagnostic criteria include hyponatremia hypoglycemia delayed tendon reflexes hypothermia altered mental status and

Present presence of a prevalent in a precipitating event like infection lab testing again includes thyroid stimulating hormone and t4 caught cortisol levels prior to giving

T4 you have a risk of schmidt syndrome which is an autoimmune destruction of both adrenal and thyroid glands what is a schmidt syndrome

Autoimmune destruction of both adrenals and thyroid gland so look for the precipitation in ecg labs septic work and ct head treatment is airway management fluid

Resuscitation thyroid hormone replacement general supporting measures and treatment of the precipitating illness t4 is given even if tsh is unknown now alternate alternative to rapidly

Correcting young critical ill patients you can give t3 hydrocarbon is given prior to giving t4 decreased metabolism after thyroxine administration can deplete cortisol levels and lead to adrenal insufficiency

Central hypothyroidism with acth deficiency so as we already talked about schmidt syndrome is an autoimmune destruction of both the adrenal and the thyroid glands is a relative adrenal insufficiency

Which is unmasked by stress and enhanced clearance of cortisol hydrocortisone is given 50 to 100 milligrams iv 6 to 8 hourly other management includes airway which could be a partial

Obstruction from macroglossia and supraglottic edema myopathy of respiratory muscles and central hyperventilation most require endotrophic intubation and long ventilatory support

To give fluids for hypotension and passive rewarming for hypothermia this is a chart summarizing the treatment of maximal hormone you can again pause your video and just have a good look

How about the treatment of mixing imacoma most of things we've already covered including protecting the airway fluid resuscitation thyroid replacement steroids collecting electrolytes and

Warming the patient okay so without thyroid hormone replacement and vigorous approach the mortality can be more than 80 with rapid treatment and iso care it falls to less than 20 percent

Some of the factors that predict a poor outcome include advanced age body temperature lesson 32 refractory hypothermia hypotension and pulse lesson 44 common mistakes is when you don't think

Of hypothyroidism you do an active rewarming rather than passive you're not treating the infection you're treating the hypotension with vasopressors rather than iv

Fluids and if it's not better in 24 hours you should look for alternative etiology like meningitis all right case three got a 58 year old lady with history of asthma emphysema and mild heart failure

Who takes methyl british loan and presents with altern mental status fever tachycardia to kepnia she's transferred from an outside hospital the family reports that she increased

Her dose herself last month because it makes her feel better given that she has been coughing and wheezing and they don't know how many pills she takes a day or when her last dose was but her bottle

Is empty sooner than it should be fever breaks after acetaminophen labs and the radiology are pending but patient remains hypotensive despite five liters of fluids adrenaline infusion is then started but

There is contrary continued refractory hypotension this is how the ecg looks like and this is 45 minutes after arrival into the hospital okay so this is a case of adrenal

Insufficiency again looking at the hypothalamus pituitary axis which is the crux of all the thyroid and adrenal problems okay so cree etiologies are primary adrenal gland destruction

So adrenal addison's disease autoimmune adrenaline and globally it is destroyed by tuberculosis disseminated infection can cause this problem so blastomycosis toxoplasmosis histoplasmosis

Then can have infiltration of the adrenal gland which can lead to adrenal destruction like incorporate sarcoma cancers are most commonly metastases from the lung and the breast cancer

It can also be idiopathic it's going to be infarction or hemorrhage post-operative congenital hydrogen hypoplasia and some drugs then you can also have secondary

Adrenal failure so like in pituitary gland where there's no acts coming from the pituitary to produce adrenal hormones pituitary apoplexy she hands syndrome which is postpartum

Hypotension traumatic brain injury can lead to this deficiency you can have this as a functional in critically ill patients with inability to mount an adequate acth and cortisol

Response to sepsis fifty percent of patients with septic shock have some degree of relative adrenal insufficiency it's associated with sepsis

Hepatic failure severe acute pancreatitis and trauma progression of adrenal crisis is underlying adrenal insufficiencies addison's and chronic steroids are an acute precipitation which can

Lead to adrenal crisis underlying adrenal insufficiency can be addisons of chronic steroid use and precipitants can be surgery anesthesia procedures infection drugs hypothermia

Adrenal hemorrhaging infection can happen in sepsis which is known as waterhouse refrigeration syndrome as in meningococcal sepsis trauma or surgery blood thoraco abdominal trauma

Is involved in heparin excessive use or used during some stress all right so key features include position weakness fatigue weight loss anorexia early psychiatric symptoms shock

Decrease or even potassium metabolic abnormalities this is a summary of uh adrenal if insufficiency hyper pigmentation is very very correct stick in adrenal insufficiency

So what happens is adrenocorticotrophic hormones it shares the precursor with melanocyte stimulating hormone all right so investigate you do electrolytes cortisol ac th

And look for the precipitant on the ecghs x-ray labs urine analysis and you do a tox panel including alcohol levels relax like the arrangement is important

Because adrenal gland failure can lead to decreased aldosterone and sodium abnormalities cortisol deficiency leads to increased adh in free water now although aldosterone is not

Deficient in secondary adrenal insufficiency increased adhd secretion alone results in hyponatremia and about 50 of the patients due to aldosterone deficiency

Hyperkalemia is in about two thirds of the patients with primary adrenal insufficiency you have hyperchlorimic metabolic alkyl acidosis it accompanies increased potassium due

To impaired exchanges sodium with hydrogen and potassium and aldosterone is deficient a cause entropion or ecth stimulation test random cortisol is less than 20

Micrograms per deciliter on a simulation test can be performed any time of the day baseline causal then 250 micrograms acts iv bolus repeat the serum cortisol levels

At 30 or 60 minutes post ac th cortisol is more than 20 micrograms and this later to exclude the diagnosis an acutely ill patient the site the physiologic stress should result in elevation of the serum

Cortisol regardless of the time of the day since the random level is adequate cortisol below 15 microns per deciliter is evidence of hypoadrenalism

So this is a summary of how do you diagnose a hypoadrenal strains this is very very important to understand to manage these problems and identify these problems carefully so physiological stress dose is 200

300 milligrams and then your replacement strategy includes 50 to 100 milligrams iv six to eight hours and the measures will improve the blood pressure and clinical picture over four

To six hours other management includes correct the electrolytes fluid resuscitation dextrose for hypoglycemia and then address a precipitating factor

Like infection or other illness this is a summary of uh hypo adrenalism treatment so maintenance maintenance and minor illness coverage during stress and what happens and what you should do in adrenal crisis

All right so corticosteroids stress dosing who when and how much is very very important so who needs a stress steroids addison's chronic pregnancy and chronic heal steroids

When like laceration suturing collis fracture reduction cardioversion for atrial fibrillation trauma septic shock and how much effective exogenous steroids is

Basically a hypopituitary adrenal access suppression hpa suppression it has occurred with any root of administration adrenal suppression may last for up to a year after a course

Of steroids hpa excess recovers quickly after penny's loans 50 probably only for five seven days this is one of the papers published looking at the pituitary adrenal

Recovery following a five-day pregnancy loan treatment so who needs steroid stress dosing all patients with known adrenal insufficiency all patients on chronic steroids equivalent to a greater

Than prednisone 5 milligram per day some other papers i've looked at it so actu stimulation test two patients on chronic pregnancy slow and premised on less than five milligram per day

No patients had suppressed hp excess in the study and three had immediate responses burnished alone more equivalent to five milligram per day found to have 50 percent had suppressed

Hba access 25 were intermediate and 25 had normal response so what duration of premise loan is important what about intermittent steroids what about inhaled

Steroids corticosteroids stress dosing in summary of literature review is short course of steroids are safe many studies in literature documented safety of britney salon for five to ten days

Some of the literature is as here so 1990 will wins mayor said 15-day course apprenticeship is safe in 1999 saw case said there's a documented hp access suppression in majority of the

Patient receiving prenatal on 10 milligram per day for four weeks many studies documenting hp excess suppression with zero news for more than one month inhale steroids looked at ellen was

Looked at by alan 2002 who looked at safety of inhaled steroids and they said adrenal suppression has occurred in moderate doses of inhaled steroids adrenal suppression

Is more common and should be considered with chronic high doses of steroids all right so there's no consistent evidence to reliably predict what dose in duration of steroid

Treatment will lead to hps suppression why now the bottom line is you consider the potential for adrenal suppression chronic pregnancy alone five milligrams per day or equivalent for an island 20 milligrams per day for

One month within the last year more than three courses of perennial and 50 milligram per day for five days within the last year chronic high dose inhale steroids so when are stressed steroids required

When stress dosing required any local procedure with duration less than one hour that doesn't involve general anesthesia or sedatives does not require stress dosing any illness

So any illness and more significant procedures require stress dosing so minor stress model stress and major stress the minor stress you do a double chronic steroid dose for duration

Of illness moderate hydrocortisone 50 milligrams per orally or iv eight hourly major 100 milligrams iv eight hourly so what about procedural sedation stressors just before the sedation the

Procedure recommended by an article in 2002 but no supporting literature specific to procedural sedation it should be done the hydrocortisone 50 milligram iv just before the procedure and then continue

With normal steroid dose so recognize key features pattern of underlying disease and the precipitant emergency management and consider corticosteroid stress

Dosing i know it's been a long lecture guys but hope you like the lecture and keep coming back for more you

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