Case PresentationUzair Ahmed

Chief Complaints

20 years old female, known case of Type I Diabetes Mellitus, came to OPD on 06-06-14 with complaints of

•Abdominal pain for 1 day•Nausea and Vomiting 1 day•Productive Cough for 1 week•No history of fever

History of Presenting Complaints• According to attendant, the patient was alright 1 day

back when she suddenly developed abdominal pain, nausea and vomiting.

• She also complained of cough with sputum which was

yellow in color. Sputum did not contain any blood and

it was not foul smelling. Cough was mild in intensity,

no specific time of occurrence, no aggravating or

relieving factors. It was not associated with chest pain,

shortness of breath or fever.

Systemic Review• Respiratory System: hx of productive cough with small amount of

yellow sputum.

• CVS: no breathlessness, palpitation or chest pain.

• GIT: Nausea and vomiting. Abdominal pain.

No heart burn, diarrhea, constipation, hematemesis or melena

present .

• CNS: Drowsiness.

• GENITO-URINARY: Polyuria but no hx of burning micturition or

incontinence was present.

• MUSCULO-SKELETAL: Normal

PAST MEDICAL HISTORY: She was diagnosed as Type I DM at

age of 9 years. Since then she had been on a regimen of Regular

and NPH insulin.

She had history of multiple hospital admission with very similar

complaints.

Past Surgical History : Nothing significant

Drug History: Insulin R+N

8+6 in Morning

6+4 in Evening

PERSONAL HISTORY: decreased appetite, decreased sleep,

normal bowel habits. No addiction. Increased Micturition.

FAMILY HISTORY: Nothing significant

SOCIO-ECONOMIC HISTORY: Poor.

Clinical Examination

Examination• Young healthy female of average built and height lying

comfortably on bed, oriented to time place and person.

• VitalsGCS 15/15B.P. 90/60Pulse 100bpmTemp A/FR/R 24

• On Examination there was no evidence of anemia, jaundice ,

clubbing or edema.• Mild to moderate dehydration was present.• No Palpable lymph nodes.

Systemic Examination

• Abdominal Exam :

Mild Tenderness at Epigastric and Left

Hypochondriac region. No visceromegaly.

• CNS Examination : Intact

• Respiratory System:

Chest was clear with NVB.

R/R was increased.

• CVS: S1+S2+0

Case Summary• 20 years old female, k/c of Type I DM, compliant to

insulin, comes to Emergency with complaints of nausea, vomiting and abdominal pain for 1 day. She has decreased appetite, increased thirst and polyuria. Her vitals shows that she has hypotension along with tachycardia and increased Respiratory Rate.

• O/E she is dehdyrated, and there is tenderness in epigastric and left hypochondriac region. Rest of the examination is unremarkable.

• There is also prior hx of hospital admissions with similar complaints.

Differential Diagnosis?

•Diabetic Ketoacidosis•Acute Pancreatitis •Acute Appendicitis•Lactic Acidosis•Metabolic Acidosis•Myocardial Infarction

Investigations (06-06-14)

• RBS: 465 mg/dl• Serum Ketones: +++

ABGs:• pH: 7.2• HCO3: 4• PaCO2: 11• PaO2: 140• SaO2: 99

LFTs:• SGPT: 31• Al.Phos: 194

• BUN: 16• Cre: 1.0• Na:132• K:4.9• Cl: 94

Anion gap• [Na+K]-[HCo3+Cl]• [132+4.9]-[4+94]• 38.9

CBC:• Hb: 13.1• TLC: 13600• MCV: 82.1• HCt: 37.8• Platelets: 270000

Investigations(contd.)

Urine D/R:•Amorphous urates : +•Ketone bodies: ++•Pus cells: 4-6•pH: 6.0•Spec. Gravity: 1.010•Glucose: ++•Yeast cells: +++•Urobilin: -ve

Investigations(contd.)

•CXR PA view was done which was found to be normal.

•ECG was performed, which was also normal.

•U/S whole abdomen was done which showed hypoechoic liver while the rest of abdomen was normal.

•Hyperglycemia(RBS=465

mg/dl)•Blood pH=7.2•Serum Bicarbonate = 4•Serum Ketones +++

Requirement to confirm DKA Our Findings

DKA Confirmed!

Treatment given:• Inf. N/S to replace the ECF fluid loss.• Inf. 5% dextrose to replace ICF fluid loss.• Insulin was administered continuously through infusion

pump initially @5units/ hour and then at 3units/hour .• Potassium was replaced.• Injection Ceftriaxone was given to cover up infection if

there were any.• Inj. Gravinate was given to treat nausea and vomiting.• RBS , BP & TPR was recorded hourly along with strict

I/O charting.• Patient clinically improved with the given treatment

and was discharged on her 6th day of admission.

Hospital CourseAt time of Admission At time of Discharge

ABGs

• pH: 7.2• HCO3: 4• PaCO2: 11• PaO2: 140• SaO2: 99

UCE • BUN: 16• Cre: 1.0• Na:132• K:4.9• Cl: 94

Anion Gap

38.9

Serum Ketones

+++

Urinary Ketones

+++

ABGs

• pH: 7.44• HCO3: 23.9• PaCO2: 32• PaO2: 171• SaO2: 99.6

UCE • BUN: 3• Cre: 0.4• Na:137• K:3.9• Cl: 105

Anion Gap

12

Serum Ketones

-

Urinay Ketones

-

Topic Discussion

Diabetic Ketoacidosis

•Definition•Etiology and Epidemiology•Pathogenesis•Diagnosis

-clinical assessment- lab investigations-Essentials for diagnosis

•Treatment

Definition:• Diabetic ketoacidosis (DKA) is an acute, major,

life-threatening complication of diabetes. DKA mainly occurs in patients with type 1 diabetes, but it is also not uncommon in some patients with type 2 diabetes.

• Also It can be the very initial presentation of the previously undiagnosed patients with Type I DM.

• This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria.

Etiology• The most common scenarios for diabetic ketoacidosis

(DKA) are underlying or concomitant infection (40%), missed insulin treatments (25%), and newly diagnosed, previously unknown diabetes (15%). Other associated causes make up roughly 20% in the various scenarios.

Causes of DKA• in type 1 diabetes mellitus

• In 25% of patients, DKA is present at diagnosis of type 1 diabetes due to acute insulin deficiency. 

• Poor compliance with insulin • Bacterial infection and

intercurrent illness (eg, urinary tract infection [UTI], vomiting)

• Medical, surgical, or emotional stress

• Idiopathic

• In type II diabetes mellitus

• Intercurrent illness (eg, myocardial infarction, pneumonia, prostatitis, UTI)

• Medication (eg, corticosteroids, pentamidine, clozapine)

Epidemiology• DKA accounts for 50% of diabetes-related admissions in young

persons and 1-2% of all primary diabetes-related admissions.• The incidence of DKA is higher in whites because of the higher

incidence of type 1 diabetes in this racial group. • The incidence of diabetic ketoacidosis (DKA) is slightly greater

in females than in males for reasons that are unclear.• Recurrent DKA frequently is seen in young women with type 1

diabetes and is caused mostly by the omission of insulin treatment.

• Among persons with type 1 diabetes, DKA is much more common in young children and adolescents than it is in adults. DKA tends to occur in individuals younger than 19 years, but it may occur in patients with diabetes at any age.

PathophysiologyInsulin is a peptide hormone, produced by beta cells in thepancreas, and is

central to regulating carbohydrate and fat metabolism in the body.Some of its physiological effects are

- Decreases blood glucose concentration by 1. increasing its uptake in the tissues

2. increasing glycogenesis3. inhibiting gluconeogenesis and glycogenolysis

- Increases uptake of aminoacid from blood into the cells and increases protein syntesis.

- Decreases blood fatty acid and ketoacid formation by stimulating fats deposition in adipose tissue and inhibiting lipolysis.

- Decreases blood K+ concentration by shifting then from ECF to ICF.

Or in a nut shell, Insulin decreases concentration of glucose, FFAs, AAs and K+ levels in blood.

Diagnosis:• Clinical Assessment:

Symptoms •Polyuria, thirst •Weight loss •Weakness •Nausea, vomiting •Leg cramps •Blurred vision •Abdominal pain

Signs• Dehydration •Hypotension (postural or supine) •Cold extremities/peripheral cyanosis •Tachycardia •Air hunger (Kussmaul breathing) •Smell of acetone •Hypothermia •Confusion, drowsiness, coma (10%)

• Lab Findings:

i. Hyperglycemia-Glucose ranges from 250-1000 mg/dl.

ii. Dilutional hyponatremia -Glucose overrides sodium in controlling the osmotic gradient. Water shifts out of the intracellular fluid compartment into the extracellular fluid compartment and dilutes the serum sodium.

iii.Hyperkalemia- Transcellular shift as excess H+ions enter

cells in exchange of potassium.iv. Increased anion gap metabolic acidosis.

-Due to ketoacidosis and lactic acidosis.v. Prerenal azotemia

-Due to volume depletion from osmotic diuresis which decreases cardiac output and renal blood flow.

• Essentials for diagnosis

Workup:

•The following are important but should not delay the institution of intravenous fluid and insulin replacement:

• Venous blood: for urea and electrolytes, glucose, bicarbonate. • Arterial blood gases to assess the severity of acidosis. • Urinalysis for ketones. • ECG. • Infection screen: full blood count, blood and urine culture, C-reactive protein, chest X-ray. Although leucocytosis invariably occurs, this represents a stress response and does not necessarily indicate infection.

Management & Treatment:Diabetic ketoacidosis is a medical

emergency which should be treated in hospital, preferably in a high-dependency area.The principal components of treatment are:

• fluid replacement • the administration of short-acting (soluble)

insulin • potassium replacement • the administration of antibiotics if infection is

present.

•Fluid Replacement:

•0.9% saline (NaCl) i.v. • 1 L over 30 mins • 1 L over 1 hr • 1 L over 2 hrs • 1 L over next 2-4 hrs

•When blood glucose < 15 mmol/L (270 mg/dL) • Switch to 5% dextrose, 1 L 8-hourly • If still dehydrated, continue 0.9% saline and add

5% dextrose, 1 L per 12 hrs •Typical requirement is 6 L in first 24 hrs but fluid overload in elderly patients should be avoided.•Subsequent fluid requirement should be based on clinical response including urine output

Insulin:

• 50 U soluble insulin in 50 mL 0.9% saline i.v. via infusion pump ▫6 U/hr initially ▫3 U/hr when blood glucose < 15 mmol/L (270

mg/dL) ▫2 U/hr if blood glucose < 10 mmol/L (180 mg/dL)

• Check blood glucose hourly initially; if no reduction in first hour, rate of insulin infusion should be increased

• Aim for fall in blood glucose of 3-6 mmol/L (approximately 55-110 mg/dL) per hour

Potassium:

•None in first L of i.v fluid unless plasma potassium < 3.0 mmol/L

•When < 3.5 mmol/L, give 20 mmol/hr •When plasma potassium is 3.5-5.0

mmol/L, give 10 mmol/hr

Additional Procedures:

• Catheterisation if no urine passed after 3 hrs • Nasogastric tube to keep stomach empty in

unconscious or semiconscious patients, or if vomiting is protracted

• Central venous line if cardiovascular system compromised, to allow fluid replacement to be adjusted accurately

• Plasma expander if systolic BP is < 90 mmHg or does not rise with i.v. saline .

• Antibiotic if infection demonstrated or suspected • ECG monitoring in severe cases .

Complications of DKA:•Cerebral oedema

▫May be caused by very rapid reduction of blood glucose, use of hypotonic fluids and/or bicarbonate

▫High mortality ▫Treat with mannitol, oxygen

•Acute respiratory distress syndrome•Thromboembolism •Disseminated intravascular coagulation (rare) •Acute circulatory failure

Prognosis:

•The overall mortality rate from DKA ranges from 1-10% of all DKA admissions. The presence of deep coma at the time of diagnosis, hypothermia, and oliguria are signs of poor prognosis.

•The prognosis of properly treated patients with diabetic ketoacidosis is excellent, especially in younger patients if intercurrent infections are absent.