DKA and Hypoglycemia

Supervised by : Dr.Mahir Ali Altala

By:
Qudama Zain Alabdeen Hassan
Ghasaq Mohammed
Fatima Subhi Mageed
Lubna Haitham Abdulhamed

Here is where our presentation begins

Table of contents

01 Diabetic ketoacidosis

02 Hypoglycemia
 01

Diabetic Ketoacidosis
Overview
Diabetic ketoacidosis (DKA) is a medical emergency and remains a serious cause of
morbidity, principally in people with type 1 diabetes.

Mortality in DKA is most commonly caused in children and adolescents by cerebral

edema, and in adults by hypokalemia , acute respiratory distress syndrome and
comorbid conditions such as acute myocardial infarction, sepsis or pneumonia.

DKA is characteristic of type 1 diabetes and is often the presenting problem in newly
diagnosed patients . However, an increasing number of patients presenting with DKA have
underlying type 2 diabetes. This appears to be particularly prevalent in black and non-
Hispanic populations.
In established type 1 diabetes, DKA may be precipitated by an intercurrent illness
because of failure to increase insulin dose appropriately to compensate for the stress
response.

Sometimes, there is no evidence of a precipitating infection and DKA develops because

of errors in self-management.
Pathogenesis

A clear understanding of the biochemical basis and pathophysiology

of DKA is essential for its efficient treatment.The cardinal biochemical features
are:

• Hyperketonaemia (" 3.0 mmol/L) or ketonuria (more than2+ on standard urine

sticks)

• Hyperglycaemia (blood glucose " 11 mmol/L (approximately200 mg/dL))

• Metabolic acidosis (venous bicarbonate<15mmol/L and/or venous pH<7.3

(H+>50nmol/L)).
Pathogenesis
 The hyperglycaemia causes a profound osmotic diuresis leading to
dehydration and electrolyte loss, particularly of particularly of sodium and
potassium.

 Potassium loss is exacerbated by secondary hyperaldosteronism as a result

of reduced renal perfusion.

 Ketosis results from insulin deficiency ,exacerbated by elevated

catecholamines and other stress hormones, leading to unrestrained lipolysis
and supply of FFAs for hepatic ketogenesis.

When this exceeds the capacity to metabolise acidic ketones, these

accumulate in blood. The resulting metabolic acidosis forces hydrogen ions
into cells, displacing potassium ions.
Pathogenesis

The average loss of fluid and electrolytes in moderately sever

DKA in an adult is :

• Water: 6 L 3L extracellular
• Sodium: 500 mmol – replace with saline
• Chloride: 400 mmol 3 L intracellular
• Potassium: 350 mmol – replace with dextrose
Pathogenesis

 Every patient in DKA is potassium-depleted but the plasma concentration of

potassium gives very little indication of the total body deficit.

 The magnitude of the hyperglycaemia does not correlate with the severity of
the metabolic acidosis; moderate elevation of blood glucose may be
associated with life threatening ketoacidosis.

 Type 1 diabetes in pregnancy is one situation where DKA can occur with
blood glucose levels that are not especially high.
Clincal feature
Symptoms
• Polyuria, thirst
• Leg cramps
• Weight loss
• Blurred vision
• Weakness
• Abdominal pain
• Nausea, vomiting

Sign
• Dehydration
• Hypotension (postural or supine)
• Cold extremities/peripheral
• cyanosis
• Tachycardia
• Air hunger (Kussmaul breathing)
• Smell of acetone
• Delirium, drowsiness, coma
Investigations
Venous blood:
for urea and electrolytes,
glucose, bicarbonate and
acid–base status
Arterial blood gases
For hydrogen ion concentration
Infection screen Urine or blood analysis
full blood count, blood For ketons
and urine culture,
C-reactive protein,
chest X-ray.
Although leucocytosis
invariably occurs in
DKA, this represents
a stress response and
does not necessarily
Indicate infection.
Electrocardiogram
Indicators of severe diabetic ketoacidosis
• Blood ketones > 6 mmol/L
• Bicarbonate < 5 mmol/L
• Venous/arterial pH < 7.0 (H+ > 100 nmol/L)
• Hypokalaemia on admission (< 3.5 mmol/L)
• Glasgow Coma Scale score < 12
• O2 saturation < 92% on air
• Systolic blood pressure < 90 mmHg
• Heart rate > 100
Emergency management of DKA

Mx
Emergency management of DKA
 Time:0-60 minutes
Establish IV access, assess patient and perform initial investigations
• Commence 0.9% sodium chloride:
If systolic BP > 90 mmHg, give 1 L over 60 mins
If systolic BP < 90 mmHg, give 500 mL over 10–15 mins, then re-assess; if BP remains < 90 mmHg, repeat and
seek senior review.

• Commence insulin treatment:

Short acting regular insulin continuous and adequate levels of circulating insulin. IV administration is usually
preferred (0.1 units/kg of regular insulin per h)
•Continue with SC basal insulin analogue if usually taken by patient.

•Establish monitoring schedule :

Hourly capillary blood glucose and ketone testing
Venous bicarbonate and potassium after 1 and 2 hrs, then every 2 hrs for first 6 hrs
Plasma electrolytes every 4 hrs
Clinical monitoring of O2 saturation, pulse, BP, respiratory rate and urine output every hour
Emergency management of DKA
 Time:60m-6h
IV infusion of 0.9% sodium chloride with potassium chloride added as indicated below:
1 L over 2 hrs
1 L over 2 hrs
1 L over 4 hrs
1 L over 4 hrs
1 L over 6 hrs

• Add 10% glucose 125 mL/hr IV when glucose < 14 mmol/L (252 mg/dL)
• Be more cautious with fluid replacement in older or young people, pregnant patients and those with renal or
heart failure;

Adjust potassium chloride infusion :

Plasma potassium(mmol/L)

• <5.5 Nil
• 3.5-5.5 20-40
• <3.5 Potassium replacement before insulin
Emergency management of DKA
 Time:6-12h
• Clinical status, glucose, ketonaemia and
acidosis should be improving;
request senior review if not
• Continue IV fluid replacement
• Continue insulin administration
• Assess for complications of treatment (fluid
overload, cerebral oedema)
• Avoid hypoglycaemia
 Time:12-24h
• By 24 hrs, ketonaemia and acidosis should have resolved
(blood ketones < 0.3 mmol/L, venous bicarbonate > 18
mmol/L)
• If patient is not eating and drinking:
Continue IV insulin infusion at lower rate of 2–3 U/hr
Continue IV fluid replacement and biochemical monitoring
• If ketoacidosis has resolved and patient is able to eat and
drink:
Re-initiate SC insulin with advice from diabetes team; do not
discontinue IV insulin until 30 mins after SC short-acting
insulin injection
Emergency management of DKA
 Despite a bicarbonate deficit, bicarbonate replacement is not usually necessary. In
fact, theoretical arguments suggest that bicarbonate administration and rapid reversal
of acidosis may impair cardiac function, reduce tissue oxygenation, and promote
hypokalemia.

 The results of most clinical trials do not support the routine use of bicarbonate
replacement, and one study in children found that bicarbonate use was associated
with an increased risk of cerebral edema. However, in the presence of severe
acidosis (arterial pH <7.0), sodium bicarbonate (50 mmol [meq/L] in 200 mL of sterile
water with 10 meq/L KCl per h) may be administered for the first 2 h until the pH is
>7.0.
Complications
1-Cerebral edema: might be due to very rapid reduction of
glucose level, use of hypotonic fluid or bicarbonate.

2-ARDS

3-DIC

4-Thromboembolism

5-Acute circulatory failure

Prognosis
 With appropriate therapy, the mortality rate of DKA is low (<1%) and is
related more to the underlying or precipitating event, such as infection or
myocardial infarction.
 Venous thrombosis, upper GI bleeding, and acute respiratory distress
syndrome occasionally complicate DKA.
 The major non-metabolic complication of DKA therapy is cerebral edema,
which most often develops in children as DKA is resolving.

 Following treatment, the physician and patient should review the sequence
of events that led to DKA to prevent future recurrences.
 70

02
Hypoglycemia
Overview
Hypoglycemia is defined as a recorded blood glucose concentration lower than normal.
Plasma glucose is maintained on a day-to-day basis within a narrow range of 72 to 144
mg/dL (4 to 8 mmol/L) by several hormonal and neural factors

•Clinically
significant hypoglycemia is rare and is based on the demonstration of Whipple triad:
signs and symptoms of hypoglycemia, in the presence of a low plasma glucose concentration
(<45 mg/dL), that are relieved by restoration of plasma glucose to normal concentrations.

•When hypoglycemia develops in non-diabetic people, it is called 'spontaneous'

hypoglycaemia
Clincal feature

Autonomic Neuroglycopenic
• Sweating • Delirium
• Trembling • Drowsiness
• Pounding heart • Speech difficulty
• Hunger • Inability to concentrate
• Anxiety • Incoordination
• Irritability, anger

Non-specific
• Nausea
• Tiredness
• Headache
Clincal feature
•Symptoms differ with age; children exhibit behavioral changes (such as naughtiness or
irritability), while elderly people experience more prominent neurological symptoms such as visual
disturbance and ataxia

•Nocturnal hypoglycaemia in patients with type 1 diabetes is probably common and under-
recognised. As hypoglycaemia does not usually waken a person who is asleep and the usual
warning symptoms are not perceived, it is often undetected. However, on direct questioning,
patients may admit to poor quality of sleep, morning headaches, 'hangover', chronic fatigue and
vivid dreams or nightmares. Sometimes a partner may observe profuse sweating, restlessness,
twitching or even seizures.

•Exercise-induced hypoglycaemia occurs in people with well-controlled, insulin-treated diabetes

because of hyperinsulinaemia and the absence of the capacity to suppress secretion of
endogenous insulin, a key factor in the normal adaptation to exercise.
Causes

• Missed, delayed or inadequate meal

• Unexpected or unusual exercise
• Alcohol
• Errors in oral anti-diabetic agent(s) or insulin dose/schedule/administration
• Poorly designed insulin regimen, particularly if predisposing to nocturnal
hyperinsulinaemia #feb300
• Lip hypertrophy at injection sites causing variable insulin absorption
• Gastroparesis due to autonomic neuropathy
• Malabsorption, e.g. coeliac disease
• Unrecognized other endocrine disorder, e.g. Addison's disease
• Factitious (deliberately induced) •
• Breastfeeding by diabetic mother
Risk factor

• Strict glycaemic control

• Impaired awareness of hypoglycaemia
• Age (very young and elderly)
• Increasing duration of diabetes
• Sleep
• C-peptide negativity (indicating complete insulin deficiency)
• History of previous severe hypoglycaemia
• Renal impairment
• Genetic, e.g.angiotensin-converting enzyme(ACE)genotype .
Glycemic Thresholds

• Within the physiologic plasma glucose range, a drop in glucose to less than 80 mg/dL
(4.5 to 4.6 mmol/L) results in decreased insulin secretion. At levels slightly lower than
the normal range, 70 mg/dL (3.6 to 3.8 mmol/L), secretion of the insulin counter-
regulatory hormones occurs: glucagon and epinephrine at 68 mg/dL, growth hormone
at 60 mg/dL, and cortisol at 60 mg/dL (3.2 mmol/L).
• The glycemic threshold for symptoms of hypoglycemia is about 54 mg/dL (3 mmol/L)
.
and, for cognitive dysfunction, about 47 mg/dL (2.6 mmol/L).

• These glycemic thresholds vary in response to the level of glucose control,

particularly in patients with diabetes; poorly controlled diabetes with persistent
hyperglycemia results in higher glucose thresholds, whereas lower glucose thresholds
are reset after single or repeated hypoglycemic episodes
Morbidity of severe hypoglycemia in diabetic patients

CNS Impaired cognitive function, Coma, Convulsions, Intellectual

decline
Transient ischaemic attack, stroke, Brain damage, Focal
neurological lesions

Heart Cardiac arrhythmias ,Myocardial ischaemia

#feb300

Eye Vitreous haemorrhage, Worsening of retinopathy

Other Accidents (including road traffic accidents), Hypothermia

Management of hypoglycemia

I. Acute intervention to prevent and minimize neurological damage.

II. Maintenance therapy to prevent recurrence of hypoglycemia .
III. subsequent measures to search for and treat the underlying cause

#feb300
Management of hypoglycemia
I. Acute intervention
Obtain blood glucose concentration as soon as possible (usually with a meter and strips, if
available):

 For symptomatic patient known to have diabetes and with a low glucose value, <70
mg/dL, administer treatment. If a glucose test cannot be performed, do not delay.
Treat as if hypoglycemia has been confirmed.
 If the glucose is low (<55 mg/dL) and the patient is a not a diabetic, draw blood for
glucose, insulin, C-peptide, and an oral hypoglycemic agent screen and then treat
 If the patient has a history of malnutrition or chronic alcohol abuse, intravenous (IV)
thiamine at a bolus dose of 12 mg/kg should be given before initiation of glucose
treatment, to avoid precipitating Wernicke’s encephalopathy.
Management of hypoglycemia
 Treatment for all hypoglucemic event’s is the administration of glucose.

 The route and amount of administration will depend on the glucose level as well as the
patient’s level of consciousness and available access.
 IF the patient is conscious able to drink and swallow safely , oral carbohydrate should be
administered urgently, followed by careful blood glucose monitoring.
 Consider the ‘rule of 15s’ during therapy (i.e. 15 g of carbohydrate will raise the glucose level
about 15 mg/dl in about 15 minutes).
Management of hypoglycemia

 Failure of the hypoglycemia to correct within 15 minutes following one dose of glucose should
lead to administration of a second dose, and occasionally a third, But failure thereafter should
prompt the clinician to consider other interventions
 IF the patient has altered mental status, is unable to swallow,give an IV bolus of 25-50 ml
(i.e.12.5-25 g) 50% dextrose ,measure a blood glucose 10 to 15 minutes after the IV bolus

 IF Iv access is not available, or is delayed, glucagon 1mg IM (or SC) can be administered, but
its action is short lived
Management of hypoglycemia
II. Maintenance therapy

 Once the glucose has been corrected, it will maintenance glucose by mouth or IV.

 The bolus of glucose should be followed by the continuous infusion of 5% to 10% glucose
(rarely, 20% to 30%) at a rate sufficient to keep the plasma glucose level greater than 100
mg/dL.
 The requirement of 8 to 10 g of glucose per hour to prevent recurrent hypoglycemia
.
 When the patient is capable of eating, a diet with a minimum of 300 g of carbohydrate per day
should be supplied.
 Oral glucose,followed by a snack containing carbohydrate and protein, if the patien has to wait
more than 30 minutes for the next meal
Management of hypoglycemia
III. Subsequent measures
 After initial stabilization,subsequent management should be directed at searching for the
underlying etiology of hypoglycemia and preventing further attacks .

 Once the underlying cause is established, definitive therapy should be offered.

 IF the hypoglycemia is a secondary process, such as from hepatic or renal failure, or

sepsis, treatment of the underlying disorder will resolve the hypoglycemia
 IF the hypoglycemia results from an insulinoma, surgical removal of the tumor is the
treatment of choice.

 Recurrent hypoglycemia in patients with diabetes requires a multidisciplinary intervention

with attention to detail at every level of management, including education, nutritional
advice, frequent glucose monitoring (including CGMS), and physiologic insulin and oral
agent therapy (including administration technique)
Thank you for listening