CASE PRESENTATION

By: Naffisah bt Othman Mohd Afiq Adli b Murad Nor Nabilla bt Khairudin Siti Nurulismah bt Che Haron Sharifah Nazeera bt Syed Anera Mas Nadiah Rasiqah bt Mustafa

Supervisor: Prof Dr Alam Sher Malik

By: Mohd Afiq Adli b Murad

DEMOGRAPHIC DETAILS
Name Gender Date of birth Age Ethnic Date and Time of Admission Date of Clerking Ward of Admission Informant Reliability Address : Khayattri A/P Segar : Female : 16/06/1996 : 14years old : Indian : 25/08/2010 at 1.30pm : 25/08/2010 at 4.30pm : Ward 8C : Mother : Good : Batu 2, Kuala Selangor

PRESENTING COMPLAINTS
Khayattri, 14 yr old Indian girl was admitted to HSB on 25th August 2010 with a complaint of frequent vomiting one day prior to admission with known history of diabetes mellitus type 1.

HISTORY OF PRESENTING COMPLAINTS

Vomiting The patient was previously well with only little episode of vomiting. The event started about 10pm on the day before been admitted. Watery, cleared vomitus with no solid and non-bilious. The vomitus was counted about a cup. She did take medication in order to relieve her condition but it tend to persist. No event of post-tussive vomiting, or vomiting after eating.

SYSTEMIC REVIEW
Respiratory system Cardiovascular system Shortness of breath, No cough, no chest pain, no hemoptysis, no wheezing Shortness of breath, no leg swelling

Central nervous system

Skin

Gastrointestinal system

Frequent headache on frontal area, no blurring of vision, no fits, no weakness of numbness of her limbs. No lumps, only having suprapubic rashes and itchiness for past 1 week No diarrhea, no constipation, no stomach ache

Genitourinary system

No menarche

No abnormal or limitation in movement, no pain, stiff and swollen joints, no muscle wasting. Hematology & Lymphatic system No bruises, no bleeding tendency, no enlargement of lymph nodes.

Musculoskeletal system

PAST MEDICAL HISTORY

She been diagnosed for having Diabetes Mellitus type 1 since she was 3 years old at Hospital Tanjung Karang, Kuala Selangor. Do have diabetic diaries, recorded for blood glucose check and also time for bolus insulin jabs. With multiple time been admitted to the hospital, previously been admitted due to hypoglycemia or frequent vomiting. Lastly been admitted, in Jun 2010 because she was fatigue and faint due to hypoglycemic. Take medication prescribed by GP for her diabetic management.

DRUG HISTORY
Bolus insulin jabs which are lispro and aspart been prescribed for her diabetic management.

ALLERGY
No food allergy. No known drug allergy.

PRENATAL HISTORY
Her mother was well during this pregnancy. No medication or drug taken during this period.

BIRTH HISTORY
Full term pregnancy She was born with normal spontaneous vaginal delivery in Hospital Kuala Lumpur. Birth weight: 2.5kg No history of neonatal jaundice and no history of admission to NICU.

FEEDING HISTORY
She is on adult diet and the whole family only take less sugar diet.

IMMUNIZATION HISTORY
Completed up to her age

DEVELOPMENTAL HISTORY
Developmental milestones have corresponding to her chronological age Able to read, count and write

FAMILY HISTORY
DM type 2 DM type 2

DM type 2

DM type 2

45Y School Bus Driver DM type 2

42Y Cleaner

16 Y

15 Y

14 Y

11y

Khayattri DM type 1

Her siblings are well and no consanguinity between her parents.

SOCIAL HISTORY
Form 2 student. She is average in her class. Involved in police cadet . She was not active in sports. Good behavior towards her teachers and peers and they do know about her condition, watch for her condition at school.

HISTORY OF CONTACT
No history of any contact.

By : Nor Nabilla bt Khairudin

General Condition
The patient was lying supine and propped up 90o. She looked drowsy and lethargic. She was conscious and alert to person, place and time She was attached to: 1. 2 branulas, which were on her right cubital fossa and the other one was on the dorsum of her left hand. 2. ECG lids on her chest. 3. Nasal prong

General Condition cont..

She was connected to : 1. 2 IV drips which were Sodium Choride and Sodium Chloride with Dextose 2. Bolus insulin 3. Humidified O2 supply She was vomited a few times and there was a yellow biohazard plastic beside her which contained her vomitus.

General Condition cont..

Her looked to be dehydrated. Her lips was dry, but no sunken eyes and good skin turgor.

No abnormal movement

Vital Signs
1. Pulse : 128 beats per minute, regular rhythm, normal volume and no collapsing pulse : 21 breaths per minute : 37.20C : 141/76 mmHg

2. Respiratory rate 3. Temperature 4. Blood pressure

Anthropometry
1. Weight : 58 kg

2. Height
3. BMI

: 148 cm
: 26.479

Examination of Face, Head & Neck, Limbs

The face was not dysmorphic, the conjunctiva was not pale and no yellowish discoloration of the sclera. No lymph nodes palpable over the neck and occipital area. There was no clubbing.

Examination of Face, Head & Neck, Limbs cont..

The palm was dry, warm, and not pale. No pitting oedema No tremor noted.

All peripheral pulses were present.

Examination of The Back

There was no abnormality of the spine. No sacral oedema.

Examination of The Lymph Nodes

No lymph nodes were palpable at the cervical,occipital and inguinal areas.

Systemic Examination

Respiratory System
Inspection: No gross deformities of the chest. The chest moves symmetrical with each respiration. There were 2 ECG lids attached to her chest. She was in kussmaul breathing. No surgical scars and no dilated veins. Palpation: The trachea was centrally located. The apex beat was located on left 5th intercostal space. Chest expansion was normal. The chest move symmetrical bilaterally,vocal fremitus was normal.

Respiratory System cont..

Percussion: The lung was resonant. Liver and cardiac dullness were present. Auscultation: Normal vesicular breath sound with good air entry. No added sound.

Cardiovascular system
Inspection: The chest shape was normal. It moved symmetrical with each respiration. No surgical scar, no dilated veins, no pericardial bulge and no visible pulsation. Palpation: The apex beat was located on left 5th intercostal space at midclavicular line. There was no palpable heave and thrill. All the peripheral pulses are present.

Cardiovascular system cont..

Percussion Normal cardiac dullness
Auscultation S1 and S2 were heard. No added sound

Abdominal examination
Inspection: The abdomen was not distended. Moved symmetrical with each respiration. The umbilicus was inverted and centrally located. There was no surgical scar, no dilated veins, and no visible pulsation and peristalsis. Palpation: The abdomen was soft and non tender. No masses palpable.

Abdominal examination cont..

Percussion: Normal resonant sound of the abdomen. Shifting dullness and fluid thrill were negative.
Auscultation: Presence of bowel sounds

Central Nervous System

1. Mental status: conscious and alert 2. Speech: no abnormality detected 3. Cranial nerves: all are intact

Central Nervous System cont..

Motor system

Muscle bulk: good muscle bulk, no areas of wasting.

Muscle power: 5/5

Muscle tone: normal tone for both limbs on both side

Reflexes: all present

Involuntary movement: nil

Sensory: Intact

Summary
Khayattri 14 years old Indian girl presented with frequent vomiting one day prior to admission with known history of diabetes mellitus type 1. She also got difficulty in breathing. On physical examination she looked drowsy, lethargic, dehydrated, tachycardic and in kussmaul breathing.

Provisional Diagnosis
DIABETIC KETOACIDOSIS known case of DM type 1
Vomiting Kussmaul breathing Dehydrated tachycardia Drowsy, Lethargic

Differential Diagnosis
HYPOGLYCEMIA
Support Multiple admission for hypoglycemia Vomiting Drowsy, Lethargic She is on bolus insulin jabs Against No tremor, sweating, palpitation, anxiety

Differential Diagnosis
HYPERGLYCEMIC HYPEROSMOLAR STATE

Support Dehydration tachycardia Drowsy, lethargic Against More common in DM type 2 Vomiting & kussmaul respiration are absent in HHS No stupor/coma

INVESTIGATIONS
Full blood count Renal Profile Serum electrolytes Venous blood Gases

a) Full Blood Count Indication: To monitor the general condition of the patient and screen the patients status and if there is any abnormal cell count.
INVESTIGATION
White cell counts Red blood cell Haemoglobin PCV MCV MCHC Platelet count

25/8/2010
16.13 x10/L 4.99 x10^6/L 12.6 g/dL 42.1 % 84.4 fl 30.0 pg/cell 538x10/L

NORMAL RANGE
4.0-5.0 x10/L

REMARKS
Increase

4.0-5.2x10^6/L 11.1-14.1 g/dL 30-45% 70-90 fl 30-36 pg/cell 110-450x10/L

Normal Normal Normal Normal Normal Increase

Impression : Increased white cell and platelet count may indicated infection in this patient.

b) Differential counts Indication: To look at which types of white blood count is elevated to rule out different types of infections.
AUTOMATED DIFFERENTIAL Neutrophil count
Lymphocyte count Monocyte count Eosinophil count Basophil count

25/8/2010 13.25 x10/L

2.26 x10/L 0.28 x10/L 0.04 x10/L 0.06 x10/L

NORMAL RANGE 1.9-8.0 x10/L

0.9-5.2 x10/L 0.16-1.0 x10/L 0.16-1.0 x10/L 0.16-1.0 x10/L

REMARKS Increase
Normal Normal Normal Normal

Impression: Increase level of neutrophil count suggestive of acute infection.

c) Renal profile Indication: To assess the renal function

INVESTIGATION Urea Sodium Potassium 25/8/2010 5.5 mmol/L 141 mmol/L 5.20 mmol/L NORMAL VALUE 2.5-6.4 mmol/L 135-145 mmol/L 3.5-5.5 mmol/L REMARKS Normal Normal Normal

Chloride
Creatinine

113.0 mmol/L
111.5 mol/L

98-107mmol/L
10-79 mol/L

Normal
Normal

Impression: No abnormalities detected

d) Venous Blood Gases Indication : To assess acid base status in blood

INVESTIGATION Blood pH pCO2 25/8/10 7.14 13mmHg NORMAL RANGE 7.35-7.38 44-48mmHg REMARKS Decrease Decrease

pO2 HCO3
O2 saturation Base Excess

147mmHg 9.4mmol/L
98.3% -22.0mmol/L

40-50mmHg 22-29mmol/L
95-100% -

Increase Decrease
Normal Abnormal

Impression : Metabolic acidosis shows by decrease in pH and decrease bicarbonate concentration. As a compensatory mechanism, respiratory alkalosis occur thus results in decrease in partial pressure of CO2. Base excess means that 22mmol/L of buffer has been used up to neutralize metabolic acids.

e) Chem Path Indication : To assess metabolic biochemistry profiles.

INVESTIGATION Calcium C-Reactive Protein Glucose Random Hemoglobin A1C Phosphate Magnesium 25/8/10 2.30 mmol/L 1.5 mg/dL 15.0 mmol/L 10.8% 0.92 mmol/L 0.95mmol/L NORMAL RANGE 2.10-2.6 mmol/L <1.0mg/dL 4.4-8.0 mmol/L <6.5% 0.8-1.45mmol/L 0.7-1.0mmol/L REMARKS Normal Increase Increase Increase Normal Normal

Impression : Hyperglycemia shows by increase in blood glucose and HBA1C. Serum C-reactive protein elevated due to acute infection.

MANAGEMENT OF DIABETIC KETOACIDOSIS

By Sharifah Nazeera

Principles of management of DKA

Fluid replacement
Intravenous solutions to replace extravascular and intravascular fluids losses. And also to dilute both the glucose level and the levels of circulating counterregulatory hormones.

Potassium replacement
Because the absence of insulin can lower the level of several electrolytes in the blood. Potassium replacement should be started with initial fluid replacement if potassium levels are normal or low.

Insulin therapy
Given intravenously to lower glucose levels and prevent further ketone production.

Fluid replacement

Bolus infusion
20ml/kg of normal saline in the first hour

Correction of 10% dehydration

deficit in ml = wt (kg) x % dehydrated x 10

Maintenance fluid
100 ml/kg for the first 10 kg. 50 ml/kg for the next 10 kg. 20 ml/kg for any weight after 20 kg.

Potassium replacement

Potassium is typically added to IV fluids to correct total body depletion of this important electrolyte. Add 20-40 mEq/L of KCl to each liter of fluid once K+ is under 5.5 mEq/L. Bicarbonate typically is not replaced since acidosis will improve with the above treatments alone.

Insulin therapy

Insulin infusion (0.05-0.1 units/kg/hr), titrating the dose according to the blood glucose. Do not give iv bolus insulin cerebral edema. Monitor the blood glucose regularly. Aim for gradual reduction of blood glucose of about 2mmol/hour, as rapid reduction is dangerous.

Actual management
1st bolus : 1.5L normal saline in 1.5 hours 2nd bolus : 1L normal saline in 1 hour Correct 10% dehydration : IV normal saline 113ml/hr for 48 hours. Maintenance fluid : IV normal saline 91ml/hr Potassium replacement : add 1g of KCl to each pint of maintenance fluid IV insulin infusion : 5.4ml/hr IV cefuroxime 1.5g TDS for 7 days Tablet PCM 1g PRN

PATHOPHYSIOLOGY OF DIABETIC KETOACIDOSIS

By : Siti Nurulismah bt Che Haron

Hyperketonemia

Hyperglycemia

Metabolic acidosis

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Etiology
For patient with known history of Diabetes Mellitus type 1: a. Stop/reduce their dose of insulin medication b. Presence any form of stress including infection, trauma or surgery c. No obvious precipitating cause

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emedicine & davison's clinical medicine

 Hypoperfusion to renal Renal secrete aldosterone

Aldosterone
Sodium retention Potassium wasting

Intracellular shift Between H+ and K+

Dehydration

Hyperkalemia

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emedicine & davison's clinical medicine

Khayattri
History Vomiting Difficulty in breathing Headache Suprapubic rashes Physical examination Drowsy Lethargic Dehydrated Tachycardic Kussmaul breathing

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Why?

Vomiting: Precipitated by production of prostaglandin Dehydrated: Hyperglycemia lead to osmotic diuresis Difficulty in breathing/Kussmaul Breathing: Compensatory mechanism to reduce metabolic acidosis Drowsy: Because of hypovolemic condition

Lethargic: Because of hypovolemic condition

Tachycardia: Heart try to compensate fluid loss Headache: Because of hypovolemic condition

Suprapubic rashes: Prone to get infection because of Diabetes Mellitus

Conclusion
Etiology
Diabetes Mellitus Type 1 She did not stop/reduce her insulin intake She did not took more than usual amount of foods/drinks Infection at suprapubic area Infection is a form of stress that may increasing glucose requirement of cells to fight it

Clinical features
Vomiting Difficulty in breathing Headache Drowsy Lethargic Dehydrated Tachycardic

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LITERATURE
10910-06.pdf SaudiJKidneyDisTranspl2058313723006_102030.pdf University Hospitals Bristol, UK.pptx

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