Acute complications of diabetes mellitus

ACUTE COMPLICATIONS OF
DIABETES MELLITUS

Questions
• A 39 year old Male patient presented to you in emergency
department for Acute Abdomen with H/O
vomiting,Restlessness,Lethargy,dehydration.On palpation of
abdomen diffuse tenderness+,no guarding/rigidity.On
Auscultation Bowel sounds heard. On eliciting History you
detect the patient is a known diabetic and is on insulin and
because of frequent travelling he is poorly complaint with
insulin.Your first probable diagnosis
a)Acute cholecystitis
b)Perforative peritonitis
c)Diabetic Ketoacidosis
d)Intestinal Obstruction

Questions
• A 62 yr old Diabetic Male presented to the Emergency with H/O fever,Right
Hypochondrial Pain,tachycardia for 2 days.CT abdomen done image is shown
below
The possible diagnosis
a)Emphysematous nephritis
b)Emphysematous cholecystitis
c)Perforative peritonitis
d)Alcoholic pancreatitis

Questions
• A 42 yr old Male known Diabetic for past 11 years with HbA1C 10.0
referred from an ENT surgeon to you the physician as a case of chronic
otorrhea,otalgia with hearing loss and now presenting with facial
asymmetry a provisional diagnosis of Rt. Facial N. palsy is made. You
suspect an infective pathology.The Probable organism could be
a)Streptococcus pneumonia
b)Hemophilus influenza
c)Pseudomonas aeruginosa
d)Clostridium perfringens

Questions
• A 54 yr old lady who is a diabetic for 12 years brought with h/o orbital cellulitis,6th
Nerve palsy and anosmia presenting with the following clinical picture
the Drug of choice for this patient?
a)Piperacillin Tazobactem
b)Amphotericin B
c)Mitomycin C
d)Actinomycin D

• Diabetic ketoacidosis
• Non ketotic hyperglycemic hyperosmolar
coma
• Hypoglycaemia & Hypoglycaemic coma
• Infections

Hyperglycemia
Ketosis
Acidosis
*
Definition of Diabetic Ketoacidosis
7
DKA is defined as the presence of all three of
the following:
(i) Hyperglycemia (glucose >250 mg/dL)
(ii) Ketosis,
(iii) Acidemia (pH <7.3).
Williams textbook of endocrinology 10th edition

Role of Insulin
• Required for transport of glucose into:
– Muscle
– Adipose
– Liver
• Inhibits lipolysis
• Absence of insulin
– Glucose accumulates
in the blood.
– Uses amino acids
for gluconeogenesis
– Converts fatty acids into ketone bodies :
Acetone, Acetoacetate, β-hydroxybutyrate.

Electrolyte
LossesRenal Failure
Shock CV
Collapse
Insulin Deficiency
9
Hyperglycemia
Hyper-
osmolality
Lipolysis
FFAs
Acidosis
Ketones
CV
Collapse
Glycosuria
Dehydration

Diabetic Ketoacidosis: Pathophysiology
Unchecked gluconeogenesis  Hyperglycemia
Osmotic diuresis  Dehydration
Unchecked ketogenesis  Ketosis
Dissociation of ketone bodies into
hydrogen ion and anions

Anion-gap metabolic
acidosis
• Often a precipitating event is identified (infection, lack of insulin
administration)

Clinical Presentation of
Diabetic Ketoacidosis
History Physical Exam
• Thirst
• Polyuria
• Abdominal pain
• Nausea and/or vomiting
• Profound weakness
• Kussmaul respirations
• Fruity breath
• Tachycardia
• Dry mucous membranes
• Poor skin turgor
• Abdominal tenderness(may
resemble acute pancreatitis
or surgical abdomen)

Diabetic Ketoacidosis
PRECIPITATING EVENTS
Infection(Pneumonia / UTI / Gastroenteritis / Sepsis)
Inadequate insulin administration
Infarction(cerebral, coronary, mesenteric, peripheral)
Drugs (cocaine)
Pregnancy.
Harrison’s Principle of internal medicine 18th edition p2977

DIAGNOSIS LAB INVESTIGATIONS
Complete blood count
Serum ketones/ Urine ketones and sugar
Calculate serum osmolality and anion gap
Urinalysis and urine culture
Consider blood culture
Consider chest radiograph
Acid-base assessment

TREATMENT OF DKA
Initial hospital management
– Replace fluid and electrolytes
– IV Insulin therapy
– Watch for complications
– Treat causes
Once resolved
– Convert to home insulin regimen
– Prevent recurrence
TYPICAL BODY DEFICIT OF WATER AND ELECTROLYTES

FLUIDS
FLUID 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
extent
Insulin 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

FLUID REPLACEMENT
Administer NS as indicated to maintain hemodynamic status, then follow general guidelines:
 NS for first 4 hr.
 Consider half NS thereafter.
 Change to D5 half NS when blood glucose ≤250 mg/dL.
Hours Volume
 1st half-hour to 1 hour 1 L
 2nd hr 1 L
 3rd hr 500 mL– 1 L
 4th hr 500 mL– 1 L
 5th hr 500 mL– 1 L
 Total 1st 5 hr 3.5 - 5 L
 6th–12th hr 250– 500 mL/hr
May need to adjust type and rate of fluid administration in the elderly and in patients with
congestive heart failure or renal failure.

INSULIN MANAGEMENT
 Regular insulin 10 U i.v. stat (for adults) or 0.15 U/kg i.v. stat.
 Start regular insulin infusion 0.1 U/kg per hour or 5 U per hour.
 Increase insulin by 1 U per hour every 1–2 hr if less than 10% decrease in
glucose or no improvement in acid-base status.
 Decrease insulin by 1–2 U per hour (0.05–0.1 U/kg per hour) when glucose
≤250 mg/dL and/or progressive improvement in clinical status with decrease
in glucose of >75 mg/dL per hour.
 Do not decrease insulin infusion to <1 U per hour.

INSULIN MANAGEMENT CONTD…
 Maintain glucose between 140 and 180 mg/dL.
 If blood sugar decreases to <80 mg/dL, stop insulin infusion for no more than
1 hr and restart infusion.
 If glucose drops consistently to <100 mg/dL, change i.v. fluids to D10 to
maintain blood glucose between 140 and 180 mg/dL.
 Once patient is able to eat, consider change to s.c. insulin:
 Overlap short-acting insulin s.c. and continue i.v. infusion for 1–2 hr.
 For patients with previous insulin dose: return to prior dose of insulin.
 For patients with newly diagnosed diabetes: full-dose s.c. insulin based on 0.6
U/kg per day.

POTASSIUM REPLACEMENT
 Do not administer potassium if serum potassium >5.5 mEq/L or patient is anuric.
 Use KCl but alternate with KPO4 if there is severe phosphate depletion and patient is unable to
take phosphate by mouth.
 Add i.v. potassium to each liter of fluid administered unless contraindicated.
Williams textbook of endocrinology 10th edition p 454
Serum K (mEq/L) Additional K required
3.5 - 4.0 - 40mEq/L
3.5–4.5 - 20mEq/L
4.5–5.5 - 10mEq/L
>5.5 - Stop K infusion

-Williams textbook of endocrinology 10th edition

BICARBONATE
• Clinical trials do not support the routine use of bicarbonate replacement
• HCO3 replacement and rapid reversal of acidosis can impair cardiac function, reduce tissue
oxygenation and promote hypokalemia and hypocalcemia.
• However in presence of severe acidosis pH<6.9,in hemodynamic instability with pH<7.1 and
hyperkaemia with ecg finding bicarbonate therapy considered
• In the presence of severe acidosis (arterial pH <6.9), the ADA advises bicarbonate [50 mmol/L
(meq/L) of sodium bicarbonate in 200 mL of sterile water with 10 meq/L KCl per hour for 2 h
until the pH is >7.0].
Williams textbook of endocrinology 10th edition p456

TREATMENT OF DKA
GLUCOSE ADMINISTRATION
 Plasma glucose reaches 250 mg/dl in DKA or 300
mg/dl in HHS,
 Decrease the insulin infusion rate to 0.05–0.1
unit/kg/h (3–6 units/h),
 Add dextrose (5–10%) to the intravenous fluids.
Maintain the above glucose values until acidosis in
DKA or mental obtundation and hyperosmolarity in
HHS are resolved
Williams textbook of endocrinology 10th edition p 455

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.

ONCE DKA RESOLVED…
• Most patients require 0.5-0.6 units/kg/day
• highly insulin resistant patients
– 0.8-1.0 units/kg/day
• Give subcutaneous insulin at least 2 hours prior to weaning insulin
infusion.
Williams textbook of endocrinology 10th edition p455

CLINICAL ERRORS
Fluid shift and shock
 Giving insulin without sufficient fluids
 Using hypertonic glucose solutions
Hyperkalemia
 Premature potassium administration before insulin has begun to
act
Hypokalemia
 Failure to administer potassium once levels falling
Recurrent ketoacidosis
 Premature discontinuation of insulin and fluid when ketones still
present
Hypoglycemia
 Insufficient glucose administration.

Hyperglycemic-Hyperosmolar State (HHS)
HNC is a syndrome characterized by impaired
consciousness, sometimes accompanied by
seizures, extreme dehydration, , and extreme
hyperglycemia that is not accompanied by
ketoacidosis.

DKA HHS
Ketonemia/Ketonuria + Ketonemia/Ketonuria -
Serum Osmolality N Serum Osmolality >320mosm
pH<7.3 pH>7.3
S.Glucose >250mg/dL S.Glucose >600mg/dL

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)
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

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.

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 and it can occur at any time.

Precipitating factors
• irregular ingestion of food;
• extreme activity;
• alcohol ingestion;
• drug interaction;
• liver or renal disease;
• hypopituitarism and adrenal insufficiency.

Pathophysiology of hypoglycaemia
Inhibition of
endogenous
insulin secretion
Counter-
regulatory
hormone
release
• Glucagon
• Adrenaline
Onset of
symptoms
• Autonomic
• Neuroglycopa
enic
Neurophysiologic
al dysfunction
• Evoked
responses
Widespread
EEG
changes
Cognitive
dysfunction
• Inability to
perform
complex
tasksSevere
neuroglycop
aenia
• Reduced
level of
consciosn
ess
• Convulsio
ns
• Coma
83 mg/dL
58–50 mg/dL
68 mg/dL
54–43 mg/dL 54 mg/dL 50 mg/dL
<27 mg/dL
Arterialisedvenousbloodglucoseconcentration
(mmol/L)
2.
0
3.
0
4.
0
1.
0
0
5.
0
Cryer et al. Diabetes Care 2003;26:1902–12
EEG, electroencephalogram

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 unconscious.

Treatment
• The most effective treatment of an insulin reaction is the immediate
ingestion of a concentrated carbohydrate source, such as sugar, honey,
candy, or orange juice.
• Alternative methods for increasing blood glucose may be required when
the person having the reaction is unconscious or unable to swallow:
– Glucagon may be given intramuscularly or subcutaneously.
– In situations of severe or life-threatening hypoglycemia, it may be
necessary to administer glucose intravenously.

• BG = 40 mg%: Give
(100-40) x 0.8 = 60 x
0.8= 48 ml of IV 25%
Dextrose.
• Repeat BG q 15 mins
until BG > 70mg%.
Example • If BG < 70mg% : 25% dextrose as per
calculation. Check BG q15 mins
• If BG > 70mg% : Check BG q30 mins till
BG > 90mg%
• If BG > 90mg% : Check BG q1hrly, Hold
Infusion
• If BG > 140mg%: Restart infusion at 50%
of previous rate
BG ≤70 – Suspend Insulin, Give 25% Dextrose (100-BG) X 0.8**

Infections
Complement:
some studies have detected a deficiency of the C4 component in DM,this reduction of C4 is
probably associated with polymorphonuclear dysfunction and reduced cytokine response
Polymorphonuclear and mononuclear leukocytes:
Decreased mobilization of polymorphonuclear leukocytes, chemotaxis, and phagocytic activity
may occur during hyperglycemia.
hyperglycemic environment inhibits glucose-6-phosphate dehydrogenase (G6PD), increasing
apoptosis of polymorphonuclear leukocytes, and reducing polymorphonuclear leukocyte
transmigration
In tissues that do not need insulin for glucose transport, the increased intracellular glucose levels
are then metabolized, using NADPH as a cofactor and the low NADPH prevents the regeneration
of molecules that play a key role in antioxidant mechanisms of the cell, thereby increasing the
susceptibility to oxidative stress.
the glycated hemoglobin (HbA1c) is <8.0%, to maintain the proliferative function of CD4 T
lymphocytes and their response to antigens.

Infections• Respiratory infections
Streptococcus pneumoniae and influenza virus
• Tuberculosis
• Urinary infections
• Bacterial pyelonephritis
E.Coli & Proteus
• Emphysematous pyelonephritis
E.Coli & Proteus followed by enterobacter.
• Emphysematous cystitis
The most frequent pathogen is E. coli, followed by Enterobacter, Proteus, Klebsiella,
and Candida
• Perinephric abscess
gram-negative bacilli (predominantly E. coli) or polymicrobial infection
• Emphysematous cholecystitis
The emphysematous cholecystitis is more frequent in males with DM.The main
pathogens are Salmonella enteritidis and Campylobacter
• Invasive external otitis
Invasive external otitis is an infection of the external auditory canal that can extend to
the skull base and adjacent regions.It often affects elderly diabetic individuals and the
etiologic agent is usually Pseudomonas aeruginosa

Acute complications of diabetes mellitus

Acute complications of diabetes mellitus

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Acute complications of diabetes mellitus