Jump to comment:

• Treatment of Acute Adrenal Crisis.
  Robert James
  Published on: 18 December 2007
• Use of empirical hydrocortisone in suspected adrenal crisis
  Mark A R Jadav
  Published on: 17 October 2007
• Comments to Diabetic and endocrine emergencies
  Viktor Rosival
  Published on: 26 June 2007
• the possible role of acidosis-related capillary permeability in adult respiratory distress syndrome
  oscar,m jolobe
  Published on: 21 February 2007

• Published on: 18 December 2007

  Treatment of Acute Adrenal Crisis.

  • Robert James, MD Medicine

  Adrenal crisis is a medical emergency. If suspected treatment should be started as soon as possible. Every emergency physician should be familiar with adrenocortical insufficiency—a potentially life-threatening entity. The initial diagnosis and decision to treat are presumptive and are based on history, physical examination, and, occasionally, laboratory findings. Delay in treatment while attempting to confirm this diag...

  Show More

  Adrenal crisis is a medical emergency. If suspected treatment should be started as soon as possible. Every emergency physician should be familiar with adrenocortical insufficiency—a potentially life-threatening entity. The initial diagnosis and decision to treat are presumptive and are based on history, physical examination, and, occasionally, laboratory findings. Delay in treatment while attempting to confirm this diagnosis can result in poor patient outcomes.

  The predominant manifestation of adrenal crisis is shock, but the patients often have nonspecific symptoms such as anorexia, nausea, vomiting, abdominal pain, weakness, fatigue, lethargy, fever, confusion or coma and hyperpigmentation [3]. Hypoglycemia is a rare presenting manifestation of acute adrenal insufficiency; it is more common in secondary adrenal insufficiency caused by isolated corticotropin (ACTH) deficiency [1,2].

  Treatment consists of starting an intravenous line, taking the blood samples for plasma cortisol levels, acth, serum electrolytes and glucose. Fluid deficit should be corrected with 5 percent DNS or normal saline. Initially 2-3 litres may be required. Thereafter give IV fluids according to the central venous pressure. Patients with addisons disease have low cardiac reserve, so watch for fluid overload. Give hydrocortisone 100-300 mg IV, there after 50-100mg every six hourly for the first day. On the second day give the same amount of dose eight hourly. Then according to the clinical response. Then switch to oral hydocortisone 10-20 mg every six hours. Most patients settle with a BD dose of 10-20mg of hydrocortisone daily. A few may need mineralocorticoid therapy in the form of fludrocortisone. Instead of hydrocortisone, dexamethasome can also be used. Hydrocortisone should not be given for atleast eight hours before ACTH stimulation test. Correct the electrolyte abnormalities as per the lab reports. Broad spectrum antibiotics should be given at this time.

  1. Burke, CW. Adrenocortical insufficiency. Clin Endocrinol Metab 1985; 14:947.

  2. Stacpoole, PW, Interlandi, JW, Nicholson, WE, Rabin, D. Isolated ACTH deficiency: a heterogeneous disorder. Critical review and report of four new cases. Medicine 1982; 61:13.

  3. Barnett, AH, Espiner, EA, Donald, RA. Patients presenting with Addison's disease need not be pigmented. Postgrad Med J 1982; 58:690.

  Show Less

  Conflict of Interest:
  None declared.

  • Back to top
• Published on: 17 October 2007

  Use of empirical hydrocortisone in suspected adrenal crisis

  • Mark A R Jadav, Emergency Medicine

  Editor,

  In their helpful review article, Kearney and Dang advocate giving hydrocortisone to suspected adrenal crisis pending ACTH stimulation testing. Many authorities suggest the use of dexamethasone prior to testing as it does not interfere with cortisol assay (eg. Webb et al 1999, Shenker et al 2001). Can the authors justify their postponement of confirmatory tests?

  Yours sincerely

  Mark...

  Show More

  Editor,

  In their helpful review article, Kearney and Dang advocate giving hydrocortisone to suspected adrenal crisis pending ACTH stimulation testing. Many authorities suggest the use of dexamethasone prior to testing as it does not interfere with cortisol assay (eg. Webb et al 1999, Shenker et al 2001). Can the authors justify their postponement of confirmatory tests?

  Yours sincerely

  Mark Jadav

  Kearney T and Dang C. Diabetic and endocrine emergencies. Postgraduate Medical Journal 2007:83:79-86

  Webb A, Shapiro M,Singer M and Suter P. Oxford Textbook of Critical Care. Oxford University Press 1999 p.603

  Shenker V and Skatrud JB. American Journal of Respiratory and Critical Care Medicine, Volume 163, Number 7, June 2001, 1520-1523

  Show Less

  Conflict of Interest:
  None declared.

  • Back to top
• Published on: 26 June 2007

  Comments to Diabetic and endocrine emergencies

  • Viktor Rosival, Clinical Biochemist

  Dear Editor,
  
  In the recent review "Diabetic and endocrine emergencies (1) several important issues have been omitted or incompletely explained.
  
  1. On p 79, the authors write "In DKA, the severe deficiency in insulin and increased counter-regulatory hormones lead to increased lipolysis and production of ketone bodies and resulting metabolic acidosis. It is...

  Show More

  Dear Editor,
  
  In the recent review "Diabetic and endocrine emergencies (1) several important issues have been omitted or incompletely explained.
  
  1. On p 79, the authors write "In DKA, the severe deficiency in insulin and increased counter-regulatory hormones lead to increased lipolysis and production of ketone bodies and resulting metabolic acidosis. It is not known why people with HHS do not develop ketoacidosis, but it is postulated to be owing lower level of free fatty acids or higher portal vein insulin". I am sorry, but the "severe deficiency in insulin ... resulting in metabolic acidosis" is also only "postulated". Concrete measurements in patients with DKA have shown considerable amounts of plasmatic insulin: in the monograph "Diabetic coma: ketoacidotic and hyperosmolar" (2) in the fig 6.3 on p 67 are references of 12 papers reporting such results. And according to Waldhäusl et al (3), increased counterregulatory hormones are the consequence of DKA, not its cause. Therefore, instead of "It is not known why people with HHS do not develop ketoacidosis" more probable is the opposite view "The existence of HHS is a strong evidence that severe deficiency of insulin and increased counter-regulatory hormones do not lead to metabolic acidosis".
  
  2. On the same p 79, the authors write also "Confusion is an unusual presentation for DKA" and they have completely omitted coma in DKA, its most severe and immediately life threatening stage (4).
  
  3. On p 80, in the paragraph "management", the authors write "Bicarbonate replacement in patients with DKA remains controversial as randomised control clinical trials have not been able to show a clear benefit". As mentioned in the foregoing paragraph 2, in DKA immediately life threatening is coma, due to very low blood pH (4, 5). The glycolytic enzyme phosphofructokinase is inhibited by decreasing blood pH and, thus, glucose utilisation in brain cells is impaired. The clinical consequence is drowsiness - stupor - coma - death in coma. Therefore, most important is increase of the low blood pH with infusions of alkalising solutions (and not "bicarbonate replacement"). Zero lethality of coma in DKA is reported when treatment has included also infusions of alkalising solutions, e g Wagner (6). Where are published similar reports on zero lethality without alkalising solutions?
  
  Dr. Viktor Rosival,
  SYNLAB Department of Clinical Biochemistry,
  Derer's Hospital,
  Limbová 5,
  SK-833 05 Bratislava,
  Slovakia,
  e-mail: rosivalv@hotmail.com
  
  References (1) Kearney T and Dang C. Diabetic and endocrine emergencies. Postgraduate Medical Journal 2007:83:79-86
  (2) Schade PS, Eaton Rt, Alberti KGMM and Johnston DG. Diabetic coma: ketoacidotic and hyperosmolar. Albuquerque, University of New Mexico Press, 1981
  (3) Waldhäusl W, Kleinberger G, Korn A et al. Severe Hyperglycemia: Effects of Rehydration on Endocrine Derangements and Blood Glucose Concentration. Diabetes 1979:28:577-84
  (4) American Diabetes Association, Hyperglycemic Crises in Diabetes. Diabetes Care 2004:27:Suppl 1:S94-S102
  (5) Edge JA, Roy Y, Bergomi A et al. Conscious level in children with diabetic ketoacidosis is related to severity of acidosis and not to blood glucose concentration. Pediatric Diabetes 2006:7:ll-5
  (6) Wagner A, Risse A, Brill H-L et al. Therapy of Severe Diabetic Ketoacidosis. Diabetes Care 1999:22:674-7
  

  Show Less

  Conflict of Interest:
  None declared.

  • Back to top
• Published on: 21 February 2007

  the possible role of acidosis-related capillary permeability in adult respiratory distress syndrome

  • oscar,m jolobe, retired geriatrician

  Dear Editor,

  Although adult respiratory distress syndrome (ARDS) is a complication common to both ketotic and non-ketotic diabetic decompensation (1), being arguably attributable to the development of adverse osmotic gradients which generate pulmonary oedema (2), the fact that ARDS is much commoner in diabetic ketoacidosis (DKA) than in hyperosmolar non-ketotic (HONK) diabetic decompensation (3)(4)(5) suggests that th...

  Show More

  Dear Editor,

  Although adult respiratory distress syndrome (ARDS) is a complication common to both ketotic and non-ketotic diabetic decompensation (1), being arguably attributable to the development of adverse osmotic gradients which generate pulmonary oedema (2), the fact that ARDS is much commoner in diabetic ketoacidosis (DKA) than in hyperosmolar non-ketotic (HONK) diabetic decompensation (3)(4)(5) suggests that the discrepancy in prevalence might be attributable to risk factors unique to DKA. Support for the view that acidosis may be an important risk factor comes from the documentation that the association of tachypnoea and metabolic acidosis can give rise to pulmonary oedema in the animal model of ARDS (6). In humans it has been suggested that the microangiopathy, and, hence, increased capillary permability, documented in the skeletal muscle of diabetic patients might have, as its corollary, an increase in capillary permeability in the presence of ketoacidosis (7). Accordingly, metabolic acidosis and its corollary, ketoacidosis, might be the additional risk factor rendering patients with DKA more liable than their counterparts with HONK to ARDS.

  References
  (1) Kearney T and Dang C. Diabetic and endocrine emergencies. Postgraduate Medical Journal 2007:83:79-86
  (2) Kitabachi AE and Wall BM. Diabetic ketoacidosis. Medical Clinics of North America 1995:79:9-37
  (3) Lorber D. Nonketotic hypertonicity in diabetes mellitus. Medical Clinics of North America 1995:79:39-52
  (4)Carroll P and Matz R. Adult respiratory distress syndrome complicating severely uncontrolled diabetes mellitus:report of nine cases and a review of the literature Diabetes care 1982:5:574-80
  (5) Marshall SM and Alberti KGMM. Hyperosmolar non-ketotic diabetic coma. The Diabetes Annual 1988;4:235-247
  (6) Sinha R., Tinka MA., Hizou R et al. Metabolic acidosis and lung mechanics in dogs. American review of Respiratory diseases 1972:106-881
  (7) Brun-Buisson CJL., Bonnet F., Bergeret S., Lemaire F., Rapin M. Recurrent high-permeability pulmonary edema associated with diabetic ketoacidosis. Critical Care Medicine 1985:13:55-56

  Show Less

  Conflict of Interest:
  None declared.

  • Back to top