Showing posts with label Internal-medicine. Show all posts
Showing posts with label Internal-medicine. Show all posts

Dec 31, 2018

Thyroid storm, endocrinal emergency diagnosis and treatment

Definition: Thyroid storm, is a life-threatening medical emergency in which excessive concentrations of thyroid hormone produce organ dysfunction. It is an uncommon manifestation of hyperthyroidism.
Precipitating factors:
  • Severe infection.
  • Diabetic ketoacidosis.
  • Direct trauma or surgical manipulation of the thyroid gland.
  • Iodine, either from excessive ingestion, intravenous administration, or radiotherapy.
  • Discontinuation of antithyroid medications.
  • Of interest, salicylates have been implicated in triggering thyroid storm by increasing the concentration of circulating free thyroid hormones to critical levels.

Clinical manifestation & Diagnosis

The diagnosis of thyroid storm relies heavily on clinical suspicion.

  • Thermoregulatory dysfunction---- (high fever, warm moist skin, diaphoresis)
  • Neurologic manifestations---- (mental status changes, seizure, coma, psychosis, hyperreflexia, lid lag)

Myxedema Coma| definition, causes, symptoms, diagnosis and treatment

Definition: The term myxedema coma is a misnomer, as myxedema and coma are neither diagnostic criteria nor common presenting findings. A more proper description would be critical hypothyroidism.

Precipitating factors

  • Infections, especially pneumonia, are perhaps the most common precipitating factor.
  • Cardiac events (myocardial infarction, congestive heart failure).
  • Cerebral infarction.
  • Trauma, hemorrhage.
  • Hypothermia, hypoglycemia.
  • Respiratory depression secondary to anesthetics or sedatives.

Clinical findings/ picture

  • Hypothermia
  • Hypotension
  • Bradycardia
  • Mental status depression ( common clinical feature and may progress to stupor or frank coma
  • Hypoglycemia
  • Generalized skin and soft tissue swelling and the presence of cool, dry skin.
  • Periorbital edema , ptosis, macroglossia


  • The diagnosis is suspected clinically and confirmed with TFT (elevated TSH levels and low levels of free T4 and T3)
  • The degree of TFT abnormalities does not distinguish hypothyroidism from myxedema coma. Rather, the distinction is based on clinical findings. 
  • It is important for the clinician to be able to differentiate hypothyroidism from euthyroid sick syndrome, in which patients have a reduction in both TSH and thyroid hormone levels.

Treatment of Myxedema Coma

  • Thyroid hormone replacement should be given intravenously to ensure rapid restoration of bioactive thyroxine levels and resolution of symptoms
  • High-dose intravenous thyroxine is given as a bolus of 300-500 mcg, followed by 50-100 mcg daily depending on the patient's age, weight, and risk of complications. This method provides a more rapid recovery of symptoms but carries the potential for unwanted cardiac events resulting from the rapid replacement of thyroxine.
  • In the low-dose method, thyroxine 25 mcg is given daily for 1 week followed by a gradually increased dose until the patient is able to resume normal thyroxine orally
  • Regardless of the replacement method used, all patients should be continuously monitored for hypertension and cardiac ischemia.
  • Supportive care should be provided while thyroid hormone levels are replaced. Ventilatory support, passive external rewarming, and correction of underlying electrolyte abnormalities are commonly required. 

Diabetic Ketoacidosis (DKA) definition, symptoms, diagnosis, treatement

Definition: DKA is a potentially fatal acute metabolic complication of diabetes mellitus. It is characterized by the biochemical triad of hyperglycemia, ketonemia, and metabolic acidosis.

DKA is typically associated with type 1 diabetes but may also occur in type 2 diabetes during periods of infection, trauma, cardiovascular injury, or other emergencies. It is more common in young people with type 1 diabetes and in females. It may be the presenting manifestation of diabetes.

Precipitating factors

  • Inadequate dosing of insulin
  • Cardiovascular disorders (myocardial infarction, stroke)
  • Infection.
  • Drug use (steroids, diuretics, vasopressors, antipsychotics, cocaine).


DKA results from severe alterations in carbohydrate, protein, and lipid metabolism. In simple terms, it is the consequence of severe cell starvation and death resulting from a relative or complete deficiency of insulin needed to transport glucose into the cells. Increased gluconeogenesis, increased glycogenolysis, and decreased use of glucose by the muscles, liver, and fat lead to profound metabolic derangements. Insulin deficiency promotes lipolysis. Lipolysis also plays a key role in promoting metabolic decompensation by providing the substrate for the formation of ketone bodies (acetone, beta-hydroxybutyric acid, and acetoacetic acid). Decreased clearance of ketone bodies leads to ketonemia and results in an anion gap metabolic acidosis. There are also elevated levels of proinflammatory cytokines and procoagulant factors (C-reactive protein and interleukin-6 and -8) that predispose the patient to thrombosis.

Clinical Manifestation and Diagnosis

Severe disease can develop in less than 24 hours after the onset of ketosis.Clinical manifestations include:
  • Polyuria, polydipsia, polyphagia, and weakness.
  • Manifestation of dehydration (dry mucous membranes, flattened neck veins, tachycardia, hypotension, and orthostasis).
  • Nausea and vomiting are common, occurring in up to 80% of patients.
  • A fruity odor to their breath, resulting from elevated serum acetone.
  • Kussmaul respirations (rhythmic, gasping deep respirations with normal or reduced frequency). as a compensatory response to the underlying metabolic acidosis seen in this disorder.
  • Altered mental status. The spectrum can vary from mild confusion to coma.

N.B. In short, DKA is nearly universally associated with  profound intravascular volume depletion and restoration of this is a cornerstone of therapy.


  1. Serum ketones
  2. Widened anion gap metabolic acidosis.
  3. Hyperglycemia is almost always seen but is not required for the diagnosis, and clinically significant DKA can occur in patients with normal serum glucose levels.
  4. Most patients have elevations in the blood urea nitrogen and serum creatinine concentration,
  5. Hyponatremia results from the osmotic diuresis
  6. Hyperkalemia results from insulin deficiency
  7. Hemoglobin A1C measurement may be useful in determining whether the episode is an acute exacerbation of previously controlled diabetes or the first manifestation of undiagnosed diabetes. However, level of hemoglobin A1C should not be relied on to diagnose or initiate treatment for DKA.
  8. Evaluation for underlying infectious causes should be undertaken because of the common associations with DKA.

Treatment strategies

  • Normalization of the serum glucose and electrolytes(especially in potassium, magnesium, and phosphorous).
  • Restoration of the intravascular volume.
  • Resolution of the metabolic acidosis (closure of the anion gap).
  • Treatment of the precipitating factor e.g.sepsis.



  • An initial intravenous bolus of regular insulin at 0.1 U/kg body weight
  • Followed by a continuous infusion of regular insulin at a dose of 0.1 U/kg/hour.
  • Long-acting and oral preparations should be strictly avoided during the initial treatment of this disorder as rapid fluctuations in serum glucose levels may be experienced and are more easily managed with regular insulin.
  • The insulin drip should be continued until the anion gap closes and not when the serum glucose level normalizes.
  • Glucose should initially be measured hourly, with appropriate adjustments to the insulin drip. If the serum glucose level becomes normal or low in the face of a persistently widening anion gap
  • Intravenous dextrose should be given and the insulin drip rate reduced but not stopped.

Initial fluid therapy

  • Up to 6 liters to adequately replete intracellular volume.
  • Caution must be taken during fluid repletion as rapid reduction in plasma osmolality can precipitate cerebral edema.
  • Isotonic saline is the initial resuscitative fluid of choice.

- Rate= 15-20 mL/kg/hour for the first several    hours.
- Once the serum glucose level is below 200-250 mg/dL, the fluids should be changed to one-half normal saline with dextrose (D5 1/2NS). 

N.B.   Fluid therapy &insulin infusion should be continued till normalization of anion gap (reflects recovery from metabolic acidosis).

Causes of death in Diabetic Ketoacidosis

  • Cerebral edema.
  • Shock.
  • Electrolyte abnormalities (esp hypokalemia induced by insulin therapy).
  • The underlying precipitant for DKA, especially sepsis. 


DKA is preventable complication of diabetes ,so patients must be educated about insulin compliance and encouraged to seek medical attention in the early coarse of illness. 

Correction of hypokalemia induced by insulin infusion in treatment of DKA

    Normal serum k+ -----------(3.5 - 5 meq/L)
  • Serum k+ is measured every hour during treatment of DKA
  • amount of k+ given is determined according to serum k+ level
serum k+ (meq/l)                  amount of k+ given (meq)

     < 3                                                 40
     3 - 4                                               30
     4 - 5                                               20
     5 - 6                                               10
     > 6                                                 0
Monitoring of serum k+ is continued every hour even after stoppage of  k+ administration to avoid recurrent hypokalemia

N.B. Due to hyperosmolarity of k+ solution ,it must be diluted.

Adrenal Insufficiency, Addison's disease, Addison's Crisis

Definition: Acute adrenal crisis is an extreme life-threatening manifestation of adrenal insufficiency. It occurs secondary to interruption of a normal or hyperfunctioning adrenal or pituitary gland or sudden interruption of adrenal replacement therapy.

Adrenal insufficiency can be divided into 3 categories:
  1.  chronic primary adrenal insufficiency (Addison disease)
  2.  chronic secondary adrenal insufficiency
  3.  and adrenal crisis (acute adrenal insufficiency).

Addison disease 

       causes :
  • Autoimmune in 80 % of cases
  • Infections (T.B. , HIV)
  • Metastases

 Chronic secondary adrenal insufficiency (-- ACTH)

caused by pituitary tumour

Adrenal crisis

 causes :
  • Sudden withdrawal of chronic steroids usage (or secondary to stress)
  • Adrenal hge (caused by,meningiococci-sepsis-warfarin therapy-coagulopathy)
  • Pituitary dysfunction (sheehan syndrome)
  • CNS lesions in rare cases         

Clinical manifestations of adrenal crisis

  • Unexplained hypotension (resistant to fluid and catecholamines)  
  • nonspecific symptoms such as anorexia, nausea, vomiting, abdominal pain, weakness, fatigue, lethargy, fever, confusion, or coma.


Immediate treatment of adrenal crisis should begin prior to laboratory confirmation (usually hyperkalemia,hyponatremia)

  • Normal saline is the intravenous fluid of choice
  • Stress-dose steroid replacement should be administered. Hydrocortisone may be administered as a 100-mg intravenous push followed by continuous infusion of 150-300 mg/day for 2 to 3 days
  • Alternatively, dexamethasone as a 4-mg intravenous bolus may be administered instead of hydrocortisone to avoid interference with testing of cortisol levels
  • Mineralocorticoid, namely fludrocortisone acetate, should also be administered at 0.1 mg daily. 

Mar 9, 2014

Metabolic changes and complications of Diabetes Mellitus with diagrams

This is a review of the metabolic changes that occurs in patients with D.M .
This changes are similar to that occur during fasting or starvation with the exception of hyperglycemia.
The changes are mainly due to decreased insulin action.

I- Changes in Carbohydrate metabolism :

- Decreased glucose uptake and oxidation by tissues, which produce decrease in ATP production espicially in muscles leading to muscle weakness .

- Decreased glucose utilization ( -- Glycogenesis and lipogenesis )

- Increased glucose formation ( Glycogenolysis and gluconeogenesis )
The net result is Hyperglycemia .
- Glucosuria occurs when blood glucose level exceeds 180 mg/dl (renal threshold) .

II- Changes in Lipid metabolism