Acute Complication of DM by Dr Shahjada Selim

Dr Shahjada Selim
Assistant Professor
Department of Endocrinology
Bangabandhu Sheikh Mujib Medical University, Dhaka
Email: selimshahjada@gmail.com, info@shahjadaselim.com
COMPLICATIONS OF
DIABETES MELLITUS

According to on set:
I. Acute Complications
A. Hypoglycemia
B. Hyperglycemic emergencies
Complications of Diabetes

Title
II. Chronic Complications of
Diabetes
A. Microvascular complications:
• Neuropathy, Nephropathy, Retinopathy
B. Macrovascular complications:
• Coronary artery disease, peripheral
vascular disease, stroke

According to on glycemia
I. Hypoglycemia
II. Hyperglycemic Crisis
Complications of Diabetes

DIABETES MELLITUS
Hyperglycemic
complications
Diabetic
Ketoacidosis
(DKA)
Hyperosmolar
Hyperglycemic State
(HHS)

DIABETIC KETOACIDOSIS (DKA)
Too Much
Insulin
Too Little Insulin,
Illness or Stress
Definition: A life-threatening state that results
from a relative or absolute deficiency of insulin
Hypoglycemia DKA

Definition: A life-threatening state that results
from a relative or absolute deficiency of insulin.
INSULIN
STRESS
HORMONES
Hypoglycemia Hyperglycemia
& DKA
• Usually occurs in individuals with Type 1 diabetes.
• Insulin levels are very low.
• High levels of “stress hormones”: epinephrine,
norepinephrine, growth hormone and cortisol.

PRECIPITATING FACTORS (VERY IMPORTANT):
INSULIN
STRESS
HORMONES
Hypoglycemia Hyperglycemia
& DKA
• Insufficient or no insulin.
• Physical stress: dehydration, trauma.
• Surgery, infections, heart attacks, etc.

BLOOD
GLUCOSE
80-120 mg/dL
Diabetic Ketoacidosis:
Pathophysiology
PANCREAS
Liver
FAT
MUSCLE
INSULIN
INSULIN
INSULIN-STIMULATED
GLUCOSE TRANSPORT
HEPATIC GLUCOSE
OUTPUT
INSULIN-MEDIATED
INHIBITION OF
LIPOLYSIS

Pathophysiology
PANCREAS
Liver
FAT
MUSCLE
INSULIN
INSULIN
BLOOD
GLUCOSE
HEPATIC GLUCOSE
OUTPUT
INSULIN-STIMULATED
GLUCOSE TRANSPORT
INSULIN-MEDIATED
INHIBITION OF
LIPOLYSIS
GLUCAGON

Pathophysiology
PANCREAS
Liver
FAT
MUSCLE
INSULIN
GLUCAGON
INSULIN
BLOOD
GLUCOSE
INSULIN-MEDIATED
INHIBITION OF
LIPOLYSIS
HEPATIC GLUCOSE
OUTPUT
KETONES
EPINEPHRINE,
NOREPINEPHRINE EPINEPHRINE-
STIMULATED
MYOLYSIS

Ketoacids
O=C
CH3
CH2COO- O-C-H
CH3
CH2COO-
O=C
CH3
CH3
HCO3
-
NADH
+ H+ NAD
ACETOACETATE B-HYDROXYBUTYRATE
Acetone Bicarbonate

Signs & Symptoms
HYPERGLYCEMIA
KETONES
• Polyuria and polydipsia
• Severe volume depletion
• Electrolyte depletion
• Eventual: renal hypoperfusion,
prerenal azotemia, hypotension
and shock
• Acidosis
• Compensatory resp. alkalosis
• Hypotension
• Shock

Clinical Course (Worst Case Scenario)
“Doing Well” •Precipitating Event
•Polyuria, polydipsia, dehydration
•Anorexia, nausea, vomiting, abd. pain
• Kussmal respirations, “Juicy
Fruit” Breath
•Altered consciousness
•Cardiovascular collapse
Coma &
Death

Effects on Mental Status
HYPEROSMOLALITY
HYPOTENSION
ACIDOSIS
Factors leading to impairment of CNS function:
OUCH

Consequences
• The latter observation is annoying because it
implies the following:
 The late diagnosis of type 1 diabetes in many
developing countries particularly in Africa.
 The late presentation of DKA, which is
associated with risk of morbidity & mortality
 Death of young children with DKA undiagnosed
or wrongly diagnosed as malaria or meningitis.

Diagnosis
DKA
Blood
Glucose
“Gap”
Metabolic
Acidosis
Serum
Ketones
The Diagnostic Triad of DKA:

Diagnosis
The “Anion Gap” represents the presence of
unmeasured anions.
Na+
K+
Cl-
HCO3
-
Anion Gap = Na+ - (Cl- + HCO3
-)
(Normal = 12)
Organic acids, such as acetoacetate and b-hydroxybutyrate,
decrease the HCO3
- (which is a biologic buffer) and aren’t
measured in the gap. Therefore, the gap increases.

Diagnosis of Diabetic Ketoacidosis
Signs and symptoms of DKA may be accompanied by
those of the underlying precipitating disorder;
HOWEVER,
DKA per se DOES NOT CAUSE
FEVER.
Therefore, if a fever is present, assume
there is an infection until proven
otherwise!!

DIAGNOSIS
• You should suspect DKA if a diabetic
patient presents with:
 Dehydration.
 Acidotic (Kussmaul’s) breathing, with a
fruity smell (acetone).
 Abdominal pain &or distension.
 Vomiting.
 An altered mental status ranging from
disorientation to coma.

The three major metabolic derangements in DKA
are:
• Hyperglycemia
• Ketosis
• Metabolic acidosis
• The definitive diagnosis consists of hyperglycemia
(blood glucose levels >16.6 mmo/L)
• low bicarbonate (<15 mEq/L)
• and low pH (<7.3)
• with ketonemia (positive at 1:2 dilution) and
moderate ketonuria.
Diagnosis

 Hyperglycemia leads to osmotic diuresis,
dehydration, and a critical loss of electrolytes.
 Hyperosmolality of extracellular fluids from
hyperglycemia leads to a shift of water and
potassium from the intracellular to the
extracellular compartment.
 Extracellular sodium concentration frequently is
low or normal despite enteric water losses
because of the intracellular-extracellular fluid
shift. This dilutional effect is referred to as
pseudohyponatremia.

 Serum potassium levels may be normal or
elevated, despite total potassium depletion
resulting from protracted polyuria and
vomiting.
 Metabolic acidosis is caused by the excess
ketoacids that require buffering by
bicarbonate ions; this leads to a marked
decrease in serum bicarbonate levels.

Management
The management steps of DKA includes:
Assessment of causes & sequele of DKA by
taking a short history & performing a scan
examination.
Quick diagnosis of DKA at the ER.
Baseline investigations.
Treatment, Monitoring & avoiding
complications.

Assessment
 History:
Symptoms of hyperglycemia, precipitating
factors, diet and insulin dose.
 Examination:
 Look for signs of dehydration, acidosis,
electrolytes imbalance, including shock,
hypotension, acidotic breathing, CNS status…etc.
 Look for signs of hidden infections (Fever
strongly suggests infection) and If possible,
obtain accurate weight before starting
treatment.

Quick Diagnosis
Known diabetic children confirm D
hyperglycemia, K ketonuria & A acidosis.
Newly diagnosed diabetic children be careful
not to miss because it may mimic serious
infections like meningitis.
Both Hyperglycemia (using glucometer)
glycosuria, & ketonuria (with strips) must
be done in the ER and treatment started,
without waiting for Lab results which may
be delayed.

Baseline Investigations
The initial Lab evaluation includes:
 Plasma & urine levels of glucose &
ketones.
 ABG, U&E (including Na, K, Ca, Mg, Cl,
PO4, HCO3), & arterial pH (with calculated
anion gap).
 Venous pH is as accurate as arterial (an
error of 0.025 less than arterial pH)
 Complete Blood Count with differential.
 Further tests e.g., cultures, X-rays…etc ,
are done when needed.

Pitfalls in DKA
 High WCC: may be seen in the absence of
infections.
 BUN: may be elevated with prerenal
azotemia secondary to dehydration.
 Creatinine: some assays may cross-react
with ketone bodies, so it may not reflect
true renal function.
 Serum Amylase: is often raised, & when
there is abdominal pain, a diagnosis of
pancreatitis may mistakenly be made.

Treatment
Principles of Treatment:
 Careful replacement of fluid deficits.
 Correction of acidosis & hyperglycemia via
Insulin administration.
 Correction of electrolytes imbalance.
 Treatment of underlying cause.
 Monitoring for complications of treatment.
Manage DKA in the PICU. If not available it
can be managed in the special care room of
the pediatric inpatient ward.

Fluids replacement
 Determine hydration status:
A. Hypovolemic shock: administer 0.9% saline,
Ringer’s lactate or a plasma expander as a
bolus dose of 20-30 ml/kg. This can be
repeated if the state of shock persists. Once
the patient is out of shock, you go to the 2nd
step of management.

Fluids replacement/2
B- Dehydration without shock:
1. Administer 0.9% Saline 10 ml/kg/hour for an
initial hour, to restore blood volume and
renal perfusion.
2. The remaining deficit should be added to
the maintenance, & the total being replaced
over 36-48 hours. To avoid rapid shifts in
serum osmolality 0.9% Saline can be used
for the initial 4-6 hours, followed by 0.45%
saline.

Fluids replacement/3
• When serum glucose reaches 250mg/dl
change fluid to 5% dextrose with 0.45
saline, at a rate that allow complete
restoration in 48 hours, & to maintain
glucose at 150-250mg/dl.
• Pediatric saline 0.18% Na Cl should not be
used even in young children.

Insulin Therapy
 start infusing regular insulin at a rate of
0.1U/kg/hour using a syringe pump. Optimally,
serum glucose should decrease in a rate no faster
than 100mg/dl/hour.
If serum glucose falls < 200 prior to correction
of acidosis, change IV fluid from D5 to D10, but
don’t decrease the rate of insulin infusion.
The use of initial bolus of insulin (IV/IM) is
controversial.

Insulin Therapy/2
Continue the Insulin infusion until acidosis is
cleared:
 pH > 7.3.
 Bicarbonate > 15 mmol/l
 Normal anion gap 10-12.

Correction of Acidosis
• Insulin therapy stops lipolysis and
promotes the metabolism of ketone bodies.
This together with correction of dehydration
normalize the blood PH.
 Bicarbonate therapy should not be used unless
severe acidosis (pH<7.0) results in
hemodynamic instability. If it must be given, it
must infused slowly over several hours.
 As acidosis is corrected, urine KB appear to
rise. Urine KB are not of prognostic value in
DKA.

Insulin Therapy/3
 If no adequate settings (i.e. no infusion or
syringe pumps & no ICU care which is the
usual situation in many developing
countries) Give regular Insulin 0.1 U/kg/hour
IM till acidosis disappears and blood glucose
drops to <250 mg/dl, then us SC insulin in a
dose of 0.25 U/kg every 4 hours.
 When patient is out of DKA return to the
previous insulin dose.

Correction of Electrolyte
Imbalance
 Regardless of K conc. at presentation,
total body K is low. So, as soon as the
urine output is restored, potassium
supplementation must be added to IV fluid
at a conc. of 20-40 mmol/l, where 50% of it
given as KCl, & the rest as potassium
phosphate, this will provide phosphate for
replacement, & avoids excess phosphate
(may precipitate hypocalcaemia) & excess
Cl (may precipitate cerebral edema or
adds to acidosis).

Potassium
 If K conc. < 2.5, administer 1mmol/kg of
KCl in IV saline over 1 hour. Withhold
Insulin until K conc. becomes> 2.5 and
monitor K conc. hourly.
If serum potassium is 6 or more, do not give
potassium till you check renal function and
patients passes adequate urine.

Monitoring
A flow chart must be used to monitor fluid
balance & Lab measures.
 serum glucose must be measured hourly.
 electrolytes also 2-3 hourly.
 Ca, Mg, & phosphate must be measured
initially & at least once during therapy.
 Neurological & mental state must examined
frequently, & any complaints of headache or
deterioration of mental status should prompt
rapid evaluation for possible cerebral edema.

Complications
 Cerebral Edema
 Intracranial thrombosis or infarction.
 Acute tubular necrosis.
 peripheral edema.

Cerebral Edema
Clinically apparent Cerebral edema occurs
in 1-2% of children with DKA. It is a
serious complication with a mortality of >
70%. Only 15% recover without permanent
damage.
Typically it takes place 6-10 hours after
initiation of treatment, often following a
period of clinical improvement.

Causes of Cerebral Edema
The mechanism of CE is not fully understood,
but many factors have been implicated:
 rapid and/or sharp decline in serum
osmolality with treatment.
 high initial corrected serum Na
concentration.
 high initial serum glucose concentration.
 longer duration of symptoms prior to
initiation of treatment.
 younger age.
 failure of serum Na to raise as serum
glucose falls during treatment.

Presentations of C. Edema
Cerebral Edema Presentations
include:
 deterioration of level of consciousness.
 lethargy & decrease in arousal.
 headache & pupillary changes.
 seizures & incontinence.
 bradycardia. & respiratory arrest when
brain stem herniation takes place.

Treatment of C. Edema
• Reduce IV fluids
• Raise foot of Bed
• IV Mannitol
• Elective Ventilation
• Dialysis if associated with fluid overload or
renal failure.
• Use of IV dexamethasone is not
recommended.

Hyperosmolar Hyperglycemic State
• Less common than DKA
• Seen in Type 2 DM
• Age group is often older (>65 years)
• Mortality 5-20%!
• Often present with altered level of
consciousness due to hyperosmolar state
(when sOsm > 300mosm/kg)

HHS
• Hyperglycemia, hyper osmolality and
dehydration without ketosis
• Most frequent precipitants:
• Acute Stressors (5 I’s)
• Renal Failure
• Hyperglycemic inducing medications

Precipitating Factors
• Acute stressors or illness increase the
secretion of glucagon, cortisol and
epinephrine precipitating hyperglycemia
• 5 I’s:
• Infection
• Infarction
• Insulin (compliance/omission)
• Ischemia
• Intoxication (alcohol, drug abuse)

Regulatory Hormones
• 2 main hormones responsible to
hyperglycemia and ketoacidosis
• Insulin - deficiency or resistance
• Glucagon - excess

Normal Response
• Glucose is ingested during a meal, stimulates
the release of Insulin from b-cells of the
pancreas
• Insulin action is to restore normoglycemia:
• Decreasing hepatic glucose production
• Inhibiting glycogenolysis and gluconeogensis
• Increases the skeletal muscle and adipose tissue
uptake
• Inhibits glucagon secretion and production

Treatment of Diabetic Ketoacidosis:
Don’t Let an Elevated K+ Fool You!
MUSCLE
ACIDOSIS
H+
K+ K+
During acidosis, H+ shifts into cells to
be buffered by intracellular buffers. K+
shifts out of cells in exchange.
INSULIN Rx
Treatment with insulin causes K+ to
shift back into cells, and serum K+
may drop like a rock during therapy.
K+
INSULIN
SERUM
K+
Consequently, serum K+ may be elevated
DESPITE total body K+ depletion .
SERUM
K+
Bottom Line: “As soon as you see pee, give K+!

“Watch the Gap”
O=C
CH3
CH2COO-
O-C-H
CH3
CH2COO-
O=C
CH3
CH3
HCO3
-
NADH
+ H+ NAD
Acetone Bicarbonate
Acetone is produced during the normal regeneration of bicarbonate and
is detected by most serum ketone assays. Therefore, the serum
ketones normally increase during recovery from DKA.

“Watch the Gap”
O=C
CH3
CH2COO-
O-C-H
CH3
CH2COO-
O=C
CH3
CH3
HCO3
-
NADH
+ H+ NAD
Acetone Bicarbonate
Acetone is produced during the normal regeneration of bicarbonate and
is detected by most serum ketone assays. Therefore, the serum
ketones normally increase during recovery from DKA.
Therefore, during management of DKA,
don’t watch the ketones; WATCH THE GAP!
IMPORTANT!

Treatment of Diabetic Ketoacidosis
Finally,
Diagnose and treat the
underlying precipitating
event!

DIABETES MELLITUS
Acute Metabolic
Complications
Diabetic Ketoacidosis
(DKA)
Hyperosmolar
Nonketotic Coma
(HONK)

Hyperosmolar Hyperglycemic State (HHS)
• Life-threatening metabolic disorder of extreme
hyperglycemia without ketosis.
• Typically seen in elderly with type 2 diabetes,
some of whom are previously not diagnosed with
diabetes.
• Common precipitating events: myocardial
infarction, stroke, sepsis.
• Potentially deadly: mortality may exceed 30-50%.

Hyperosmolar Hyperglycemic
State (HHS)

Hyperosmolar Hyperglycemic State (HHS)
Relative Insulin
Deficiency
HYPERGLYCEMIA
THE
VICIOUS
CYCLE OF
HONK
POLYURIA
VOLUME DEPLETION
HEMO-
CONCENTRATION

HHS
Clinical Aspects
Increasing volume depletion and
hemoconcentration may result in:
• Hyperviscosity and increased risk of thrombosis.
• Disturbed mentation.
• Neurologic Signs:
i. Focal signs, e.g., sensory or motor deficits or focal
seizures.
ii. Motor abnormalities, e.g., flaccidity , depressed
reflexes, tremor or fasciculations.
•Ultimately, without Rx, coma and death.

HHS
Treatment
• Volume correction with normal saline.
• Replacement of electrolytes.
• IV insulin.
• Diagnosis and treatment of underlying cause.
Similar to the treatment of DKA:

• 50 year male diabetic using metformin 1000
mg since 8 year became drowsy. On
examination his pulse 90 beats per minute
BP 120/80, respiratory rate 50 per minute,
chest clear. On investigation random blood
sugar 300, blood urea 20 meg, ketone body
in urine nil.
• What is your diagonosis?
• Name 3 investigation with reasons
• What is the treatment?

Diabetes Mellitus
CHRONIC COMPLICATIONS:
Microvascular and Macrovascular
Complications

Diabetes: Chronic Complications
Microvascular
Complications
Diabetic
Retinopathy
Diabetic
NeuropathyDiabetic
Nephropathy

Diabetic Retinopathy
Retinal Fundus Photographs
NORMAL RETINA
Retinal
capillaries
Macula
Optic nerve
Macular edema
Exudates
Disease Progression
New Vessel
Formation
PROLIFERATIVE
RETINOPATHYNON-PROLIFERATIVE OR
“BACKGROUND”
RETINOPATHY

EM Photograph of Plastic Cast of Retinal
Capillaries from Diabetic Retina
Microaneurysms
Exudates
•leakage of plasma proteins into
neuroretina.
Later stages of retinopathy involve death of endothelial cells
and capillary “drop out,” progressive ischemia and
proliferative neovascular changes.

Diabetic retinopathy is the leading
cause of new adult blindness in
the United States.
Remember:

Diabetic Nephropathy
Diabetic glomerulosclerosis
Diabetic glomerulosclerosis is characterized by basement
membrane thickening and mesangial cell proliferation.
Diabetic nephropathy may be diagnosed in its earliest--and
potentially, reversible--stages by detection of extremely small
amounts of albumin in the urine, so-called “microalbumin.”
This is
EXTREMELY
important!

Diabetic Nephropathy
Diabetic nephropathy is the
leading cause of renal failure
requiring dialysis in the United
States.
Remember:

DIABETIC NEUROPATHY:
Peripheral Sensory Neuropathy
Diabetic Foot Ulcer
Diabetic “Charcot Feet”
Symmetrical neuropathy is the most common:
• Primarily involving the distal extremities with
“stocking-glove” distribution.
• Sensory: decreased vibration, temperature,
proprioception.
• Initially may present with painful
paresthesias: “burning” or “pins-and-
needles” sensation. Eventually leads to
complete loss of sensation.
• Predisposed to skin breakdown and ulcer
formation and unrecognized trauma.

DIABETIC NEUROPATHY:
Autonomic Neuropathy
• Gastroparesis
• Constipation or
Diarrhea
•Cardiac arrhythmias
•Sudden Death
• Chronic edema
• Postural
hypotension
•IMPOTENCE
•Urinary retention

Diabetic Neuropathy
Diabetes is the leading cause
of non-traumatic lower
extremity amputations in the
United States.
Remember:

DIABETIC COMPLICATIONS
MACROVASCULAR COMPLICATIONS
Gangrene is 14 times more common in people with diabetes
than those without.
Coronary Heart Disease:
• Twice as common in people with diabetes.
• Occurs at an earlier age and places women at equal risk
with men.
• For MI’s: individuals with diabetes have a high initial
mortality rate and lower 5-year survival rate.
• MI’s often occur WITHOUT CHEST PAIN.
Risk of death from stroke is approximately 3 times greater for
people with diabetes than for those without.
This is
EXTREMELY
important!

DIABETIC COMPLICATIONS:
Diabetes and Pregnancy
I. Problems for the Mother:
• Insulin requirements increase, and metabolic control
often worsens during pregnancy .
• Diabetic retinopathy , and perhaps nephropathy , may
worsen.
II. Problems for the Baby:
• Infant mortality is higher in babies of diabetic mothers.
• Congenital malformations occur more frequently .
• “Big babies” (macrosomia)
• Respiratory distress syndrome (RDS) more frequent.

DIABETIC COMPLICATIONS
INFECTIONS & HEALING
• Hyperglycemia impairs immune system function and
defense against infection.
• Tuberculosis and pneumococcal pneunomia are more
common.
• Monilial (yeast) infections are extremely common and
hard to treat.
• Wound healing is delayed in individuals with diabetes.

DIABETIC COMPLICATIONS:
Screening Exams
• Retinopathy: Retina exam - annually
• Nephropathy: Urine microalbumin-to-
creatinine ratio on random urine specimen -
annually. More often if abnormal.
• Neuropathy:
-- Test vibratory sensation with 128 Hz
tuning fork - annually.
-- Foot exam (for cracks, fissures, foreign
bodies, etc.) Every visit.

Diabetic Complications
“Diabetes is a dreadful affliction,
the melting down of flesh and
limbs into urine…Life is short,
unpleasant and painful...
-- Areteus of Capadocia, 2nd C. A.D.
What can
we do???

Acute Complication of DM by Dr Shahjada Selim

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