final acute complications of diabetes mellitus
TRANSCRIPT
![Page 1: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/1.jpg)
ACUTE COMPLICATIONS OF
DIABETES MELLITUS
Dr.Sandeep yadav
![Page 2: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/2.jpg)
ACUTE COMPLICATIONS OF
DIABETES MELLITUS
![Page 3: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/3.jpg)
1)Diabetic ketoacidisis• Precipitating factors• Signs, symptoms, physical examination, laboratory findings• Treatment
2)Non ketotic hyperglycemic hyper osmolar coma• Precipitating factors• Signs, symptoms, physical examination, laboratory findings• Treatment
3)Lactoacidosis• Precipitating factors• Signs, symptoms, physical examination, laboratory findings• Treatment
4)Hypoglycemic AND Hypoglycaemic coma• Precipitating factors• Signs, symptoms, physical examination, laboratory findings• Treatment
![Page 4: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/4.jpg)
Hyperglycemia
Ketosis
Acidosis
*
Adapted from Kitabchi AE, Fisher JN. Diabetes Mellitus. In: Glew RA, Peters SP, ed. Clinical
Studies in Medical Biochemistry. New York, NY: Oxford University Press; 1987:105.
Definition of Diabetic Ketoacidosis*
4
![Page 5: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/5.jpg)
Precipitating factors of DKA
![Page 6: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/6.jpg)
• Newly Diagnosed Diabetes (Presenting Manifestation
• Inadequate Administration Of Exogenous Insulin;
ABSOLUTE INSULIN
DEFICIENCY
• Inadequate Administration Of Exogenous Insulin
• An Intercurrent Infection (Pneumonia, Cholecyctitis);
• A Vascular Disorder (Myocardial Infarction, Stroke);
• An Endocrine Disorder(hyperthyroidism, Pheochromocytoma);
• Trauma;• Pregnancy;• Surgery
RELATIVE INSULIN
DEFICIENCY
![Page 7: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/7.jpg)
7
![Page 8: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/8.jpg)
Electrolyte LossesRenal Failure
Shock CV Collapse
Insulin Deficiency8
Hyperglycemia
Hyper-osmolality
Δ MS
Glycosuria
Dehydration
![Page 9: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/9.jpg)
Lipolysis
FFAs
Acidosis
Ketones
CV Collapse
Insulin Deficiency9
![Page 10: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/10.jpg)
Electrolyte LossesRenal Failure
Shock CV Collapse
Insulin Deficiency10
Hyperglycemia
Hyper-osmolality
Δ MS
Lipolysis
FFAs
Acidosis
Ketones
CV Collapse
Glycosuria
Dehydration
![Page 11: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/11.jpg)
Diabetic Ketoacidosis: PathophysiologyUnchecked gluconeogenesis Hyperglycemia
Osmotic diuresis Dehydration
Unchecked ketogenesis Ketosis
Dissociation of ketone bodies into
hydrogen ion and anions
Anion-gap metabolic
acidosis
11
• Often a precipitating event is identified (infection, lack of insulin
administration)
![Page 12: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/12.jpg)
12
![Page 13: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/13.jpg)
Clinical Presentation of
Diabetic KetoacidosisHistory Physical Exam
• Thirst
• Polyuria
• Abdominal pain
• Nausea and/or vomiting
• Profound weakness
• Kussmaul respirations
• Fruity breath
• Relative hypothermia
• Tachycardia
• Supine hypotension, orthostatic drop of blood pressure
• Dry mucous membranes
• Poor skin turgor
13
![Page 14: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/14.jpg)
Initial Laboratory Evaluation of DKA
• Comprehensive metabolic profile
• Serum osmolality
• Serum and urine ketones
• Arterial blood gases
• CBC
• Urinalysis
• ECG
14
![Page 15: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/15.jpg)
Treatment
REFERENCES:
1) American Diabetic Association
2) British Medical Journal
3) E-medscape
4) Harisson Principle Of Internal Medicine 18th
Edition
5) British Society Of Paediatric Endocrinology
And Diabetes
![Page 16: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/16.jpg)
The goals of therapy include:
1.Rehydration
1.Reduction of hyperglycemia
2.Correction of electrolyte imbalance
3. Correction of acid-base imbalance
4.Investigation of precipitating factors, treatment of complications.
![Page 17: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/17.jpg)
FLUIDSFLUID RESUSCITATION IS A CRITICAL PART
OF TREATING PATIENTS WITH DKA. Intravenous solutions replace extravascular and
intravascular fluids and electrolyte losses. They also dilute both the glucose level and the levels
of circulating counterregulatory hormones. Fluid it self leads to correction of acidosis to some
extentInsulin is needed to help switch from a catabolic
state to an anabolic state, with uptake of glucose in tissues and the reduction of gluconeogenesis as well as free fatty acid and ketone production
![Page 18: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/18.jpg)
0.9 % NaCl(15-20 ml/kg/hr)
Administer 1-3 L during the first hour.
Administer 1 L during the second hour
Administer 1 L during the following 2 hours
Administer 1 L every 4 hours, depending on the degree of dehydration and central venous pressure readings
![Page 19: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/19.jpg)
In general, 0.45% NaCl infused at 4–14 ml · kg−1 ·
h−1 is appropriate if the corrected serum sodium is
normal or elevated
![Page 20: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/20.jpg)
INSULIN RECOMENDATIONS
![Page 21: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/21.jpg)
In adult patients, (IfK+ <3.3 mEq/l) , an IV bolus of regular insulin at 0.15 u/kg body wt
continuous infusion of regular insulin at a dose of 0.1 unit · kg−1 · h−1 (5–7 units/h in adults), should be administered
If plasma glucose does not fall by 50 mg/dl from the initial value in the 1st hour, check hydration status; if acceptable, the insulin infusion may be doubled every hour until a steady glucose decline between 50 and 75 mg/h is achieved.
When the plasma glucose reaches 250 mg/dl in DKA or 300 mg/dl in HHS, it may be possible to decrease the insulin infusion rate to 0.05–0.1 unit · kg−1 · h−1 (3–6 units/h), and dextrose (5–10%) may be added to the intravenous fluids.
Initiate subcutaneous insulin at least 2 h before interruption of insulin infusion
![Page 22: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/22.jpg)
Potassium Repletion in DKA
• K+ >5.2 mEq/L▫ Do not give K+ initially, but check serum K+ with
basic metabolic profile every 2 h▫ Establish urine output ~50 mL/hr
• K+ <3.3 mEq/L▫ Hold insulin and give K+ 20-30 mEq/hr until
K+ >3.3 mEq/L
• K+ = 3.3-5.2 mEq/L▫ Give 20-30 mEq K+ in each L of IV fluid to
maintain serum K+ 4-5 mEq/L
22
![Page 23: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/23.jpg)
Phosphorus Repletion in DKA
• A sharp drop of serum phosphorus can also occur during insulin treatment
• Treatment is usually not required
▫ Caregiver can give some K+ as K- phos
23
![Page 24: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/24.jpg)
CORRECTION OF ACID BASE BALANCE
Its role is controversial
Sodium bicarbonate only is infused if decompensated acidosis starts to threaten the patient's life, especially when associated with either sepsis or lactic acidosis
It is recommended for patients in shock and/or if pH is <6.9
![Page 25: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/25.jpg)
Treatment of Concurrent Infection
• In the presence of infection, the administration of proper antibiotics is guided by the results of culture and sensitivity studies. Starting empirical antibiotics on suspicion of infection until culture results are available may be advisable.
![Page 26: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/26.jpg)
![Page 27: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/27.jpg)
Criteria for resolution of DKA
glucose <200 mg/dl,
serum bicarbonate ≥18 mEq/l, and
venous pH of >7.3.
Once DKA is resolved, if the patient is NPO, continue intravenous insulin and fluid replacement and supplement with subcutaneous regular insulin as needed every 4 h.
![Page 28: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/28.jpg)
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.
![Page 29: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/29.jpg)
HHS
CEREBROVASCULAR
ACCIDENTS,PANCREATITIS,BURN
INFECTIONS(PNUEMONI
A,UTI)
DRUGS (STEROIDS,THIAZIDE
S)
![Page 30: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/30.jpg)
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.
![Page 31: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/31.jpg)
Laboratory findings1. 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)
3. Serum ketones are usually not detectable, and patients are not acidic.
4. Serum sodium may be high (if severe degree of dehydration is present), normal, or high
5. Serum potassium levels may be high (secondary to the effects of hyperosmolality) Low or normal
![Page 32: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/32.jpg)
DKA and HHS Are Life-Threatening
EmergenciesDiabetic Ketoacidosis (DKA)
Hyperglycemic Hyperosmolar State (HHS)
Plasma glucose >250 mg/dL Plasma glucose >600 mg/dL
Arterial pH <7.3 Arterial pH >7.3
Bicarbonate <15 mEq/L Bicarbonate >15 mEq/L
Moderate ketonuria or ketonemia Minimal ketonuria and ketonemia
Anion gap >12 mEq/L Serum osmolality >320 mosm/L
32
![Page 33: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/33.jpg)
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.
![Page 34: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/34.jpg)
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.
The hallmark of LA is the presence of tissue hypoxemia, which leads to enhanced anaerobic glycolysis and to increased lactic acid formation.
The normal blood lactic acid concentration is 1 mmol/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.
![Page 35: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/35.jpg)
Predisposing factors
1. Heart and pulmonary failure (which leads to hypoxia)
2. Alcohol intoxication.
3. Ketoacidosis (it is important to have a very high index of suspection with respect to presence of LA).
![Page 36: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/36.jpg)
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.6. Findings associated with coexisting medical
problems (e.g., renal disease, cardiovascular disease) may be evident.
![Page 37: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/37.jpg)
Laboratory findings
1. Blood glucose level is not high
2. Glucosurea is absent.
3. Blood lactic acid is high.
![Page 38: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/38.jpg)
Treatment of LA
LA is treated by correcting the underlying cause.1. Oxygentherapy2. Metyleneblue (50 – 100 ml of 1 % solution i/v
droply)3. In severe cases, bicarbonate therapy should be
used (intravenously-infused 2,5 % sodium bicarbonates 1 to 2 l/day).
4. LA can be treated with low dose insulin regimens with 5 % glucose solution infusion.
5. Symptomatic therapy:- Hydrocortisone (250 mg i/v)- Unitiol (5% solution 10 ml i/v (1- 2 ml/10 kg)- α-lipoid acid (berlition, espa-lipon)
![Page 39: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/39.jpg)
Comparison of DCA, HNC and LA.
![Page 40: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/40.jpg)
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.
![Page 41: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/41.jpg)
Precipitating factors
• irregular ingestion of food;
• extreme activity;
• alcohol ingestion;
• drug interaction;
• liver or renal disease;
• hypopituitarism and adrenal insufficiency.
![Page 42: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/42.jpg)
![Page 43: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/43.jpg)
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.
![Page 44: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/44.jpg)
Treatment
• The most effective treatment of an insulin reaction is the immediateingestion of a concentrated carbohydrate source, such as sugar,honey, candy, or orange juice.
• Alternative methods for increasing blood glucose may be requiredwhen the person having the reaction is unconscious or unable toswallow:▫ Glucagon may be given intramuscularly or subcutaneously.▫ In situations of severe or life-threatening hypoglycemia, it may be
necessary to administer glucose intravenously.
![Page 45: Final acute complications of diabetes mellitus](https://reader034.vdocuments.us/reader034/viewer/2022042716/55ac32371a28abbb4b8b4631/html5/thumbnails/45.jpg)
PREVENTION IS BEST CURE