«confirm» on methodical meeting of endocrinology department a chief of endocrinology department, prof. Vlasenko M. V. “ 31 ” august 2012 y methodological recommendations icon

«confirm» on methodical meeting of endocrinology department a chief of endocrinology department, prof. Vlasenko M. V. “ 31 ” august 2012 y methodological recommendations




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MINISTRY OF HEALTH PROTECTION OF UKRAINE

Vynnitsa national medical university named after M.I.Pyrogov





«CONFIRM»

on methodical meeting of endocrinology department

A chief of endocrinology department, prof. Vlasenko M.V.


_________________

“_31_”_august___ 2012 y



METHODOLOGICAL RECOMMENDATIONS

for independent work of students

by preparation for practical classes



Scientific discipline

Internal medicine

Мodule № 1

^ Basis of Internal medicine

substantial module №1

Diagnostic, treatment and prophylactic basis of main endocrinology diseases”


Topic

Topic №7: Comas in the patient with diabetes mellitus. Ketoacidosis. Diabetic ketoacidotic coma: pathogenesis, clinics, diagnostics, treatment. Hypoglycemic coma: pathogenesis, clinics, diagnostics, treatment. Concept about hyperosmolar and lactatacidotic comas. Features of comas in the children with diabetes mellitus.

Course

4

Faculty

Medical № 1



Vynnitsa – 2012


^ METHODOLOGICAL RECOMMENDATIONS

for the students of 4-th course of medical faculty for preparation to the practical classes from endocrinology


1.Тopic №7: Comas in the patient with diabetes mellitus. Ketoacidosis. Diabetic ketoacidotic coma: pathogenesis, clinics, diagnostics, treatment. Hypoglycemic coma: pathogenesis, clinics, diagnostics, treatment. Concept about hyperosmolar and lactatacidotic comas. Features of comas in the children with diabetes mellitus.


2. Relevance of topic: Diabetic emergencies are dangerous acute complications of Diabetes Mellitus. Contemporary diagnosis and prevention of comas determine tactic and value of treatment approach. So, this problem stimulates researchers and doctors of different specializations to improve our knowledge in this topic. Ketoacidosis is the most frequent endocrine emergency seen by the primary care physician. Mortality rates from 6 – 10 % have been reported. All the abnormalities associated with ketoacidosis can be traced to an absolute or relative insulin lack, which develops over the period of several hours or days.


^ 3. Aim of lesson:

- to learn etiology, pathogenesis, diagnostic criteria of diabetic ketoacidosis (DKA), nonketonic hyperglycemic-hyperosmolar coma (NKHHC), lactoacidosis (LA) and hypoglycemic coma (HC).

- to know how to differentiate symptoms of diabetic ketoacidosis .

- to know how to diagnose hypoglycemic coma.

- to know how to diagnose hyperosmolar state.

- to know how to interpret results of the laboratory assays.

- to know clinical picture, differential diagnosis and frst aid of diabetic emergencies.

- to learn methods of prophylaxis the comas at Diabetes Mellitus.


4. References

4.1. Main literature

  1. Endocrinology. Textbook/Study Guide for the Practical Classes. Ed. By Petro M. Bodnar: - Vinnytsya: Nova Knyha Publishers, 2008.-496 p.

  2. Basіc & Clіnіcal Endocrіnology. Seventh edіtіon. Edіted by Francіs S. Greenspan, Davіd G. Gardner. – Mc Grew – Hіll Companіes, USA, 2004. – 976p.

  3. Harrison‘s Endocrinology. Edited J.Larry Jameson. Mc Grew – Hill, USA,2006. – 563p.

  4. Endocrinology. 6th edition by Mac Hadley, Jon E. Levine Benjamin Cummings.2006. – 608p.

  5. Oxford Handbook of Endocrinology and Diabetes. Edited by Helen E. Turner, John A. H. Wass. Oxford, University press,2006. – 1005p.

4.2. Additional literature

  1. Endocrinology (A Logical Approach for Clinicians (Second Edition)). William Jubiz.-New York: WC Graw-Hill Book, 1985. - P. 232-236.

  2. Іnternatіonal Textbook of Dіabetes Mellіtus (Ed by R.A. Defronzo, E. Ferrannіnі, H. Keen, P. Zіmmet. John Wіley & Sons, Ltd. England, 2004. – Vol. 1 – 1100p., Vol. 2 – 1913p.

  3. Joslіn’s Dіabetes Mellіtus. Selected Chapters from the 14-th ed. Edіted by C. Ronald Kahn, et al. Lіppіncott Wіllіams & Wіlkіns, USA, 2006. – 328p. Manual of Endocrinology and Metabolism (Second Edition)/ Norman Lavin. – Little, Brown and Company.- Boston-New York-Toronto-London, 1994. - P. 519-527, 561-574.

  4. The diabetic foot. 2nd edition. Edited by A.Veves, J.M.Giurini, F.W. LoGerfo (ebs), Humana Press, Totowa, New Jersey,2006. – 224p.



Basic Level.

  1. Pathogenesis of insulin lack.

  2. Drugs which can be used in emergency of DM patients with coma.

Students’ Independent Study Program


You should prepare for the practical class using the existing text books and lectures. Special attention should be paid to the following:

  1. Stages of DKA development.

  2. Etiology and diagnosis of diabetes ketosis.

  3. The clinical forms of duration and diagnosis of DKA.

  4. Diagnostic criteria of diabetic ketoacidosis.

  5. Diagnostic criteria of hyperosmolar coma.

  6. Diagnostic criteria of lactic acidosis.

  7. Diagnostic criteria of hypoglycemic coma.

  8. Emergency of DKA.

  9. Etiology of NKHHC.

  10. Diagnosis of NKHHC.

  11. Emergency of NKHHC.

  12. Etiology and diagnosis of LA.

  13. Emergency of LA.

  14. Etiology of HC.

  15. Diagnostic criteria of HC.

  16. Emergency of HC.

  17. Differentiate diagnosis between diabetic emergencies.



Short content of the theme.

Classification of acute complications of DM.

  1. Diabetic coma:

  1. diabetic ketoacidisis (DKA);

  2. nonketonic hyperglycemic-hyperosmolar coma (NKHHC);

  3. lactoacidosis (LA).

  1. hypoglycemic coma (HC).



Diabetic ketoacidisis (DKA).

DKA results from grossly deficient insulin modulation of glucose and lipid metabolism.

Pathophysiology of DKA.

Insulin deficiency

(absolute or relative)




↓ glucose uptake




↑ proteolysis




↑ lipolysis

























↑ aminoacides

↑ nitrogen loss

muscle breakdown






glycerol

free fatty acids








































weight loss










↑ ketogenesis








































Weakness










↑ keton

emia




























Hyperglycemia




Gluconeogenesis + glucogenolysis










↑ keton

uria



















Glucosuria


































Osmotic diuresis




Electrolyte depletion

























Hypotonic losses




Dehydration and acidosis








Precipitating factors:

  1. newly diagnosed diabetes (presenting manifestation);

  2. inadequate administration of exogenous insulin;

  3. increased requirements for insulin caused by the presence of an underlying stressful condition:

  • an intercurrent infection (pneumonia, cholecyctite);

  • a vascular disorder (myocardial infarction, stroke);

  • an endocrine disorder(hyperthyroidism, pheochromocytoma);

  • trauma;

  • pregnancy;

  • surgery.

Clinical presentation.
^

Diabetic ketosis.


It is status which is characterized by increased level of ketones in blood, without clinical signs of dehydration and can be corrected by diet (fat restriction) and regular insulin injection.

DKA develops over a period of days or weeks.

Signs and symptoms.

  1. Polydipsia, polyurea and weakness are the most common presenting complaints.

  2. Anorexia, nausea, vomiting, and abdominal pain may be present and mimic an abdominal emergency.

  3. Ileus and gastric dilatation may occur and predispose to aspiration.

  4. Kussmaul breathing (deep, sighing respiration) is present as respiratory compensation for the metabolic acidosis and is obvious when the pH is less than 7.2.

  5. Symptoms of central-nervous-system involvement include headaches, drowsiness, lassitude, stupor and coma (only 10 % patients are unconscious).

Physical examination.

  1. Hypotermia is common in DKA. A fever should be taken as strong evidence of infection.

  2. Hyperpnea or Kussmaul respiration are present and related to degree of acidosis, acetone may be detected on the breath (musty (fruity) odor to the breath).

  3. Tachycardia frequently is present, but blood pressure is usually normal unless profound dehydration is present.

  4. Poor skin tugor may be prominent depending on the degree of hydration.

  5. Hyporeflexia (associated with low serum potassium) can be elicited.

  6. Signs consistent with a “surgical abdomen” but which follow severe ketonemia can confuse the clinical picture.

  7. In extreme cases of DKA one can see hypotonia, stupor, coma, incoordination of ocular movements, fied dilated pupils, and finally death.

  8. Other signs from a precipitating illlness can be present.

Laboratory findings.

  1. The hallmark of DKA is the finding of:

  • hyperglycemia;

  • ketonemia;

  • metabolic acidosis (plasma pH and bicarbonates are decreased.

  1. A presumptive bedside diagnosis is justified if the urine is strongly positive for both glucose and ketones.

  2. Different changes of electrolyte levels in the blood can be observed and does not reflect the actual total body deficits.

  3. Serum amylase and transaminases can be elevated.

  4. Leucocytosis occurs frequently in DKA and therefore cannot be used as a sole indication of infectious process.

Types of DKA:

  • abdominal;

  • vascular collapse;

  • cerebral (encephalopathic);

  • renal;

  • mixed.

Treatment.

The goals of therapy include:

  1. Rehydratation.

  2. Reduction of hyperglycemia.

  3. Correction of: a) acid-base and b) electrolyte imbalance.

  4. Investigation of precipitating factors, treatment of complications.

The most important factor to emphasize is the frequent monitoring of the patient both clinically and chemically. Initially, laboratory data should be obtained every 1 – 3 hours and less frequently once clinical improvement is noted. If the patient is in shock, stupor or coma, a nasogastric tube, especially if vomiting, and urinary catheter are recommended.

Frequent assessment of potassium status is vital. A lead II electrocardiogram (ECG) can be provide a rapid assessment of hyperkalemia (peaked T waves) and hypokalemia (flat T waves and presence of U waves). Hyporeflexia and ileus are clinical indications of potassium deficiency.

Careful observation of neurological status is vital to detect the infrequent but devastating presence of cerebral edema.

Rehydration.

The average fluid deficit in adults with DKA is 3 to 5 l. A rapid infusion of 0,9 % sodium chloride (e.g., 1 l/h for the first 1 to 2 hours) is given and then reduced to about 0,5 – 0,3 l/h if the blood pressure is stable and the urine follow is adequate. After the initial infusion, intravenous fluid therapy must be adjusted individually on the basis of urine output, clinical assessments of hydration and circulation, determination of plasma electrolytes and glucose. When serum glucose level is about 11 – 13 mmoll/l administration of 5 % glucose with insulin can be performed (1 to 2 unites of insulin on each 100 ml of 5 % glucose solution). The addition of glucose to the intravenous solution is necessary for correction of tissue lipolysis and acidosis.

^ Insulin treatment.

DKA can be treated with low dose insulin regimens; e.g., initial intravenous administration of 10 to 20 units of regular insulin followed by continuous intravenous infusion of 0,1 unit/kg/hour in 0,9 % sodium chloride infusion. (50 units of insulin can be added to a 500 ml bottle of 0,9 % sodium chloride solution to give 1 insulin unite/10 ml of solution.)

If the glucose level does not improve after an hour of infusion, the rate of insulin is doubled until a response is noted. But if there is a tendency for decreasing the level of glucemia we have to decrease the dose of insulin in two times.

When the serum glucose concentration reaches 11-13 mmoll/l, insulin can be given subcutaneously (if plasma and urine persistently negative for ketones). Blood glucose level should be maintained at about 11 mmoll/l during intravenous therapy.

Improvement usually is noted in 8 – 24 hours. Following stabilization of the clinical condition, patients are placed in insulin regimen consisting of five injections of regular insulin.

^ Treatment of electrolyte disorders.

As a rule, potassium should never be given until the state of renal function is known and until the serum potassium concentration is available. In most patients the initial serum potassium is high-normal or elevated, and the initiation of K replacement (20 to 40 mmoll/h) usually can be deferred for 2 hours, using hourly serum measurements as a guide.

Potassium would be to infuse at a rate of ml of 1,5 g/h during 3 – 5 hours.

^ Correction of metabolic acidosis.

The metabolic acidosis occurs due to insulin deficiency and dehydration. So ketone bodies are themselves metabolized to bicarbonate once proper therapy is begun (fluids, electrolytes, insulin) and exogenous administration of bicarbonate can overcorrect to alkalosis.

The use of bicarbonate can be recommended only in the following cases:

  • if life-threatening hyperkalemia;

  • when severe lactic acidosis complicates DKA;

  • with severe acidosis (pH<7), especially when complicated by shock that is not responsive to appropriate fluid resuscitative measures in an attempt to improve cardiac output.

Bicarbonate would be to infuse at a rate of 100 to 300 ml of 2,5 % solution.

Other therapeutic consideration:

  • since infection is one of the leading precipitating events of DKA, it should be looked for and, if found, treated appropriately;

  • vascular thrombosis (it is secondary to severe dehydration, high serum viscosity, and low cardiac output) – heparin (5000 unites 4 times a day);

  • vascular collapse can be treated by mesatone (1 – 2 ml); glucocorticoides (dexametasone 4 mg two times a day). You must remember that development of vascular collapse after initiation of therapy should suggest the presence of gram-negative sepsis or silent myocardial infarction;

  • cerebral edema (It is a rare and frequently fatal complication. Some physicians believe that rapid osmotic reduction of plasma glucose should be avoided to minimize rapid osmotic changes. Some patients have premonitory symptoms (e.g., sudden headache, rapid decrease in the level of consciousness), but in others acute respiratory arrest is the initial manifestation. If cerebral edema is diagnosed, therapeutic maneuvers might include the use of : mannitol (1 – 2 g/kg intravenous over 20 min), dexametasone (0,25 – 0,50 mg/kg/day divided q 4 – 6 h). But they are usually ineffective after the onset of respiratory arrest.


^ Nonketonic hyperglycemic-hyperosmolar coma (NKHHC or HNC).

HNC is a syndrome characterized by impaired consciousness, sometimes accompanied by seizures, extreme dehydration, , and extreme hyperglycemia that is not accompanied by ketoacidosis.

The syndrome usually occurs in patients with type II DM, who are treated with a diet or oral hypoglycemic agents, sometimes it is a complication of previously undiagnosed or medically neglected DM (type II).

In contrast to ketoacidosis, mortality in patients with HNC has been very high (50 %) in most series. Mortality has been associated with convulsions, deep vein thrombosis, pulmonary embolus, pancreatitis and renal failure. Death is usually due to an associated severe medical condition and not to the hyperosmolality.

The pathophysiology of HNC is similar to that of ketoacidosis, except that ketoacids do not accumulate in the blood. The reason of this phenomenon is unclear. Initially it was thought that patients with HNC produced enough insulin to prevent lipolysis and ketogenesis but not enough to prevent hyperglycemia. The concept was invalidated by finding similar inappropriately low plasma insulin concentrations in patients with the two syndromes. The finding of lower plasma free fatty acids, as well as cortisol and growth-hormone concentrations, in patients with ketoacidosis has raised the possibility that the absence of ketosis may be the result of decreased cortisol and growth-hormone effects on lipolysis. Suppression of lipolysis by hyperosmolality also has been proposed.

HNC usually develops after a period of symptomatic hyperglycemia in which fluid intake is inadequate to prevent extreme dehydration from the hyperglycemia-induced osmotic diuresis.


^ PREDISPOSING FACTORS FOR HYPERGLYCEMIC HYPEROSMOLAR STATE

I. Acute illness

– acute infection (32–60 %)

– pneumonia, urinary tract infection, sepsis

– cerebral vascular accident

– myocardial infarction

– acute pancreatitis

– intestinal obstruction

– dialysis, peritoneal

– mesenteric thrombosis

  • renal failure

  • heart stroke

  • hypothermia

  • subdural hematoma

  • severe burns

  • acute pulmonary edema

II. Endocrine

  • acromegaly

  • thyrotoxicosis

  • Cushing’s syndrome

III. Drugs/therapy

  • β-Adrenergic blockers

  • Calcium channel blockers

  • Chlorpromazine

  • Cimetidine

  • Diazoxide

  • Diuretics

  • Ethacrynic acid

  • Immunosuppressive agents

  • L- Asparaginase

  • Phenytoin

  • Propranolol

  • Steroids

  • Total parenteral nutrition

  • Previously undiagnosed diabetes



Predisposing factors.

  1. HNC seems to occur spontaneously in about 5 – 7 % of patients.

  2. In 90 % of patients some degree of renal insufficiency seems to coexist.

  3. Infection (e.g., pneumonia, urinary tract infection, gram-negative sepsis) is underlying frequent precipitating cause.

  4. Use of certain drugs has been associated with this condition:

  • steroids increase glucogenesis and antagonize the action of insulin;

  • potassium-wasting diuretics (hypokalemia decreases insulin secretion), e.g., thiazides, furosemide;

  • other drugs, e.g., propranolol, azathioprine, diazoxide.

  1. Other medical conditions such as cerebrovascular accident, subdural hematoma, acute pancreatitis, and severe burns have been associated with HNC.

  2. Use of concentrated glucose solutions, such as used in peripheral hyperalimentation or renal dialysis, has been associated with HNC.

  3. HNC can be induced by peritoneal or hemodialysis, tube feeding.

  4. Endocrine disorders such as acromegaly, Cushing disease, and thyrotoxicosis have also been associated with HNC.

Clinical presentation.

Signs and symptoms.

  1. Polyuria, polydipsia, weight loss, weakness and progressive changes in state of consciousness from mental cloudiness to coma (present in 50 % of patients) occur over a number of days to weeks.

  2. Because other underlying conditions (such as cerebrovascular accident and subdural hematoma) can coexist, other causes of coma should be kept in mind, especially in the elderly.

  3. Seizures occur in 5 % of patients and may be either focal or generalized.

Physical examination.

  1. Severe dehydration is invariably present.

  2. Various neurologic deficits (such as coma, transient hemiparesis, hyperreflexia, and generalized areflexia) are commonly present. Altered states of consciousness from lethargy to coma are observed.

  3. Findings associated with coexisting medical problems (e.g., renal disease, cardiovascular disease) may be evident.

Laboratory findings.

  1. Extreme hyperglycemia (blood glucose levels from 30 mmoll/l and over are common.

  2. A markedly elevated serum osmolality is present, usually in excess of 350 mOsm/l. (Normal = 290 mOsm/l). The osmolality can be calculated by the following formula: mOsm/l = 2(Na + K) = blood glucose/18 + BUN/2.8.

  3. The initial plasma bicarbonate averaged.

  4. Serum ketones are usually not detectable, and patients are not acidic.

  5. Serum sodium may be high (if severe degree of dehydration is present), normal, or high (when the marked shift of water from the intracellular to the extracellular space due to the marked hyperglycemia is present).

  6. Serum potassium levels may be high (secondary to the effects of hyperosmolality as it draws potassium from the cells), normal, or low (from marked urinary losses from the osmotic diuresis). But potassium deficiency exists.

Treatment.

This condition is a medical emergency and the patient should be placed in an intensive care unit.

Many of the management techniques recommended for a patient with DKA are applicable here as well.

The goals of therapy include:

  • rehydration;

  • reduction of hyperglycemia;

  • electrolytes replacement;

  • investigation of precipitating factors, treatment of complications.

Rehydration.

The average fluid deficit is 10 liters, and acute circulatory collapse is a common terminal event in HNC. The immediate aims of treatment are to rapidly expand the contracted intravascular volume in order to stabilize the blood pressure, improve the circulation, and improve the rate of urine production. It is important to remember that it is the severe hyperglycemia and the concomitant obligatory shift of water from the intracellular to the intravascular compartment that prevents this latter space from collapsing at the time of severe fluid depletion. With too rapid a correction of hyperglycemia, potential hypovolimic shock (as fluid moves from the extracellular space back into the intracellular space) may occur.

Treatment is starting by infusion 1 to 3 liters of 0,9 % sodium chloride over 1 to 2 hours; if this suffices to stabilize the blood pressure, circulation and restore good urine flow, the intravenous fluid can be changed to 0,45 % sodium chloride to provide some free water. 0,45 % sodium chloride is used at a rate of 150 to 500 ml/hour depending on the state of hydration, previous clinical response and the balance between fluid input and output. The aim of this phase of intravenous fluid therapy is not to attempt to rapidly correct the total fluid deficit or the hyperosmolality, but rather to maintain stable circulation and renal function and to progressively replenish water and sodium at rates that do not threaten or cause acute fluid overload.

Generally, half of the loss is replaced in the first 12 hours and the rest in the subsequent 24 hours.

^ Insulin therapy.

Insulin treatment in HNC is started by 10 to 20 unites of regular insulin intravenously as a bolus dose prior to starting the insulin infusion and then giving intravenously regular insulin in a dose of 0,05 – 0,10 unites/kg/hour (many authorities routinely use the same insulin treatment regimens as for treating DKA, other authorities recommend smaller doses of insulin, because they believe that patients with type II DM are offer very sensitive to insulin, but this view is not universally accepted, and many obese type II diabetics with NHC require larger insulin doses to induce a progressive decrease in their marked hyperglycemia. It is important to remember that because of insulin therapy causes blood glucose levels to fall, water shifts into the cells and existing hypotension and oliguria can further aggravated. Thus, initially some advocate delaying insulin therapy while infusion normal saline until vital signs have improved.

When the plasma glucose reaches the range 11 to 13 mmoll/l, 5 % glucose should be added to the intravenous fluids to avoid the risk of hypoglycemia. Following recovery the acute episode, patients are usually switched to adjusted doses of subcutaneous regular insulin at 4 to 6-hour intervals. When they are able to eat, this is changed to a 1 or 2 injection regimen.

^ Treatment of electrolyte disorders.

Once urine flow has been reestablished, potassium should be added to begin repletion of the total body deficits.

Potassium replacement is usually started by adding 20 mmoll/l to the initial liter of the intravenously-infused 0,45 % sodium chloride with careful serum potassium and ECG monitoring.
^

Lactic acidosis (LA).


DM is one of the major causes of LA, a serious condition characterized by excessive accumulation of lactic acid and metabolic acidosis.

Pyruvic acid Lactic acid

NADH NAD

Acetoacetic Beta-hydroxybutyric

The hallmark of LA is the presence of tissue hypoxemia, which leads to enhanced anaerobic glycolysis and to increased lactic acid formation.

Piruvic acid is converted into lactic acid by lactic dehydrogenase (LDH) in the presence of reduced nicotinamide adenine dinucleotide (NADH), which, in turn, is converted into NAD. The reaction is reversible and involves LDH in both directions. The conversion of acetoacetic acid into beta-hydroxybutyric acid also requires the oxydation of NADH. LA results from decreased availability of NAD caused by lack of oxygen. Likewise, the deficiency of NAD impairs the conversion of beta-hydroxybutyric into acetoacetic acid. Thus, LA predisposes to accumulation of beta-hydroxybutyric acid, which does not react with acetest tablet, so, the reaction for ketone bodies may be negative or slightly positive. The normal blood lactic acid concentration is 1mmol/l, and the pyruvic to lactic ratio is 10:1. An increase in lactic acid without concomitant rise in pyruvate leads to LA of clinical importance.

Predisposing factors.

  1. Heart and pulmonary failure (which leads to hypoxia).

  2. Usage of bigyanids, pheformin therapy.

  3. Alcohol intoxication.

  4. Ketoacidosis (it is important to have a very high index of suspection with respect to presence of LA).

Clinical presentation.

Signs and symptoms.

  1. Kussmaul breathing (deep, sighing respiration) is present as respiratory compensation for the metabolic acidosis and is obvious when the pH is less than 7.2.

  2. Symptoms of central-nervous-system involvement include headaches, drowsiness, lassitude.

  3. Anorexia, nausea, vomiting, and abdominal pain may be present.

  4. Myalgia is common.

Physical examination.

  1. Acrocyanosis is common.

  2. Tachycardia frequently is present, blood pressure is decreased.

  3. Poor skin tugor and dry skin may be prominent.

  4. Hypothermia is common in LA.

  5. Hyperpnea or Kussmaul respiration are present and related to degree of acidosis.

  1. Findings associated with coexisting medical problems (e.g., renal disease, cardiovascular disease) may be evident.


Laboratory findings.

  1. Blood glucose level is not high

  2. Glucosurea is absent.

  3. Blood lactic acid is high.

Treatment.

LA is treated by correcting the underlying cause.

In severe cases, bicarbonate therapy should be used (intravenously-infused 2,5 % sodium bicarbonates 1 to 2 l/day).

LA can be treated with low dose insulin regimens with 5 % glucose solution infusion.

Volume expanders and oxygen therapy are helpful treatment as well.


Comparison of DCA, HNC and LA.




DKA

HNC

LA

Age

Below 40

Above 40

Above 40

Type of DM

Type I

Type II

Type II

Predisposing factor

Insulin deficiency

Dehydration

Hypoxia

Prodromes

Several days duration or less than 1 day

Several days duration

Less than 1 day

Underlying renal, cardiovascular or pulmonary disease

About 15 %

About 85 %

About 90 %

General

More acidic and less dehydrated, hyperventilation

More dehydrated and less acidic, no hyperventilation

More acidic and less dehydrated, hyperventilation

Neurologic symptoms and signs

Rare

Very common

Very common

Laboratory findings

- blood glucose


High (about 20 – 30 mmoll/l)


Very high (about 40 – 50 mmoll/l)


Normal or about 10 – 11 mmoll/l

- plasma ketones

+

-

-

- serum sodium

Normal, elevated or low

Normal, elevated or low

Normal

- serum potassium

Normal, elevated or low

Normal, elevated or low

Normal

- serum bicarbonate

Low

Normal

Low

- blood pH

Less than 7,35

Normal

Less than 7,35

- serum osmolality

Less than 330 mOsm/l

Over 350 mOsm/l

Normal

- free fatty acids




or normal

Normal

Complications:

  • Thrombosis

  • Mortality


Rare

1 – 10 %


Frequent

20 – 50 %


Very rare

About 90 %

Diabetes treatment after recovery

Always insulin

Diet alone or oral agents, sometimes insulin

Diet alone or oral agents, sometimes insulin

Hypoglycemia


It is a syndrome characterized by symptoms of sympathetic nervous system stimulation or central nervous system dysfunction that are provoked by an abnormally low plasma glucose level.
^

Hypoglycemia represents insulin excess and it can occur at any time.


CAUSAL FACTORS OF HYPOGLYCEMIA IN DIABETIC PATIENTS

A. Problems with insulin

I. Management errors

  • patient error

  • physician error

  • pharmacy error

  • drug interaction

  • other related conditions

(endocrine failure: Addison’s disease, Hypopituitarism, hypothyroidism)

II Altered pharmacokinetics of insulin
– change of insulin species

– change of formulation

– excessive dose

– injection: site, size, depth

– absorption: muscle exercise, massage, temperature

– delayed clearance: insulin antibodies, renal failure, hepatic failure

III. Sensitivity to insulin
– insulin antibodies
– exercise

– weight reduction

– diurnal variation

– diabetic pregnancy and following delivery

– menstrual cycle

– acute remission following treatment of type 1 diabetes

– alcohol

B. Inadequate carbohydrate – missed or delayed meals – excessive / unpremeditated exercise – delayed gastric emptying (autonomic neuropathy)

– malabsorption (coeliac disease, pancreatic exocrine failure) – slimming diets (anorexia nervosa) – pregnancy: breastfeeding


Precipitating factors.

  • irregular ingestion of food;

  • extreme activity;

  • alcohol ingestion;

  • drug interaction;

  • liver or renal disease;

  • hypopituitarism and adrenal insufficiency.

Clinical presentation.

Signs and symptoms.

Two distinct patterns are distinguished:

  1. adrenergic symptoms (they are attributed to increased sympathetic activity and epinephrine release): sweating, nervousness, tremulousness, faintness, palpitation, and sometimes hunger;

  2. cerebral nervous system manifestations: confusion, inappropriate behavior (which can be mistaken for inebriation); visual disturbances, stupor, coma or seizures. (Improvement in the cerebral nervous system manifestations will be with a rise in blood glucose.)

A common symptom of hypoglycemia is the early morning headache, which is usually present when the patient awakes.

Patients should be familiar with the symptoms of the hypoglycemia but some of them are not heralded by symptoms.

Physical examination.

  1. The skin is cold, moist.

  2. Hyperreflexia can be elicited.

  3. Hypoglycemic coma is commonly associated with abnormally low body temperature

  4. Patient may be unconsciousness.

Laboratory findings.

1. Low level of blood glucose


Common symptoms of hypoglycemia in different age groups



Children

Young adults

Elderly







Tremor

Tremor

Tremor

Hunger

Hunger




Pallor

Pounding heart

Pounding heart




Sweating

Sweating







Anxiety










Drowsiness

Drowsiness

Drowsiness

Poor concentration

Odd behaviour

Poor concentration




Confusion

Confusion

Weakness

Incoordination

Weakness

Dizziness

Speech diffculty

Dizziness

Behavioral

Nonspecifc

Neurological

Tearful

Nausea

Unsteadiness

Confusion

Headache

Poor concentration

Tiredness




Double vision

Irritable




Blurred vision

Aggressive




Slurred speech


Treatment.

Insulin–treated patients are advised to carry sugar lumps, candy, or glucose tablets at all time.

If the symptoms of hypoglycemia develop, the patients have to drink a glass of fruit juice or water with 3 tbsp. of table sugar added or to eat candy, and to teach their family members to give such treatment if they suddenly exhibit confusion or inappropriate behavior:

  1. glucagon 0,5 – 1 unit (0,5 – 1 ml) s/c, i/m or i/v. If the patient does not respond to 1 unit of glucagon within 25 minutes, further injections are unlikely to be effective, and are not recommended;

  2. an i/v injection of 20 or 100 ml of 40 % glucose, followed by a continuous infusion of 5 % glucose (10 % glucose may be needed) until it clearly can be stopped safely;

  3. glucocorticoids and adrenaline are helpful as well.



Differentiate diagnosis of diabetic comas



Clinical features

Coma




hypoglycemic

ketoacidotic

hyperosmolar

Lactic acidosis

Age

Any age

Often less than 40 y.

Often more than 40 y.

Often more than 40 y.

Eye tone

N





N

Dehydratation

-

+

++

-

Acetone breath, acetonuria

-

+

-

-

hyperglycemia

-

++

++++

+/-

glucosuria

-

++

++

+/-

Blood pressure

N







Brain edema

-

-

+/-

-

Blood osmolality

N





N

Muscle tone



N, ↓

N, ↓

N

pH of blood

N



N



Note: “-” - symptom absent, “+” - symptom present, ↑ - elevation, ↓ - decrease, N - norm.

Tests and Assignments for Self-assessment.


Multiple Choice.

Choose the correct answer/statement:

  1. A patient has been diagnosed with lactic acidosis. This condition is caused by:
  1. ^

    insulin deficiency


  2. dehydration

  3. extreme activity

  4. hypoxia

  5. intercurrent infection

  1. A patient with DKA has deep signing respiration. Kussmaul breathing is caused by:

A. hyperglycemia

B. metabolic acidosis

C. dehydration

D. hypokalemia

E. ketonemia

3. The patient of 63 years suffers from insulindependent form of diabetes. On the background of acute infringement of the cerebral cir­culation the high hyperglycemia - 56 mmol/l, severe dehydration, hyper-chloremia, hypernatremia has developed. The ketonemia and acetonuria are absent. Establish the correct diagnosis:

A. Hyperosmolar coma

  1. Acute renal failure

  2. Diabetic hyperketonemic coma

  3. Chronic renal failure

  4. Hyperlactacidemic coma

4. Patient С., 24 years with the 10-years experience of diabetes type 1 is unconsciousness, the skin is wet. Respiration is superfcial, the arterial pressure - 140/70 mmHg. Tone of muscles and tendon refexes are raised. Establish the diagnosis:

    1. Hypoglycemic coma

    2. Lactoacidotic coma

    3. Hyperosmolar coma

    4. Diabetic ketoacidotic coma

    5. Cerebral coma


Answer: 1 – D. 2 – B. 3 – A. 4 – A.


Real-life situations to be solved:

Patient D., 35 years, was hospitalized. She is unconscious. Her relatives told you, that she has type I DM and felt herself bad 3 days ago after diarrhea, when she decreased the dose of insulin. She had weakness, fatigue, nausea and vomiting. Examination: patient is unconscious, dry skin and tongue, hyporeflexia. Laboratory findings: blood glucose level – 28 mmoll/l, acetone in urine – positive. What is your previous diagnosis?

Answer: Ketoacidotic coma.


Patient F., 27 years, complains on regular morning headache, which is present when he awakes. Patient has type I DM and takes 82 units of insulin/day. What is your previous diagnosis?

Answer: Hypoglycemic status. (You have to investigate blood glucose level at 3 o’clock in the morning and if the level is low decrease the dose of insulin.)


Students Practical Activities.

Work 1 : Students’ group is divided into 2 sub-groups, that work near the patients’ bed: ask the patients on organs and systems, take anamnesis of the disease , anamnesis of life, make objective exam. With the teacher’s presence. In the class-room they discuss the patients, learn data of laboratory and instrumental exam. of these patients.

1.To group the symptoms into the syndromes.

2.To find out the leading syndrome and make differential diagnosis.

3.To formulate the diagnosis.

4.To make a plan of treatment.


Methodological recommendation prepared assistant, c.m.s. Chernobrova O.I.

It is discussed and confirm on endocrinology department meeting

" 31 " august 2012 y. Protocol № 1.

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