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Case PresentationHyperglycemia Hyperosmolar StateAngeline Maranata, dr.

RSUD Kepahiang, Bengkulu

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Patient’s Data Name: Mr. MI Age: 75 yo Sex: Male Address: Batu Bandung Religion: Moslems Marital state: Married Occupation: -

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Hospital Administration Date Hospitalised on: Dec 8th, 2015 Went out from hospital: Dec 9th, 2015

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Anamnesis Chief complaint: faint Additional complaints: slow respond to

verbal stimulus, loss appetite

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Recent Illness History (Alloanamnesis)

Patient had uncontrolled Diabetes Mellitus, Hypertension.Onset unknown

2010.Patient got stroke, right body part.

Dec 8th, 2015.Patient fainted, slow respond to verbal stimulus, and loss appetite. These complaints happened appr. 2hrs before hospitalised

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Physical Examination Vital signs

GCS: 12 (E3V4M5) HR: 100 bpm RR: 24 times BP: 170/100 mmHg Temp: 36C

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Physical Examination (2) Head to toe examination Head:

Eyes: Pale conjunctiva (-/-), icteric sclera (-/-). Pupil: direct light reflex: (-/+), indirect light reflex (-/-). Mature cataract on left

eye. Neck: lymphadenopahty (-), neck veins distention (-) Chest:

Lung: I: symmetrical chest movement P: symmetrical fremitus P: symmetrical dull A: vesicular breath sound, crackles (+/+), wheezing (-/-)

Heart I: ichtus cordis invisible P: ichtus cordis palpable on appr. Two fingers to medial left midclavicle line P: cardiomegaly undefined A: S1 and S2 normal, murmur (-), gallop (-)

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Physical Examination (3)

Abdomen: I: flat abdomen A: bowel sound (+) 6 times per minute P: tympanic sound

P: suple, tenderness (-), liver and spleen unpalpable, ballotemen unpalpable

Extremities: Right upper and lower limb atrophy. Pathologic

reflect: Babinski (-/-)

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Laboratory Findings

Emergency unit (Dec 8th, 2015) Hb: 14.1 gr/dL Ht: 36% Tr: 306.000 cell/mm3

Leu: 11.600 cell/mm3

GDS: 474 mg/dL Total Cholesterol: 174 mg/dL Uric Acid: 6.0 mg/dL Ur: 47 mg/dL Cr: 1.87 mg/dL

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Diagnosis and Management Emergency Unit

Diagnosis: Type 2 DM + Low food intake + grade II hypertension

Management: Pro: Hospitalised Diet: natrium-restricted food IVFD: I NaCl 20 drips per minute/ 8hrs MM:

Ceftriaxone vial 1gr (IV) per 12 hrs Amlodipine 2 x 5mg 1-0-1 Glimepiride 2 x 5mg 1-0-1

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Follow Up (8/12/2015) (23.30 WIB) Bangsal S: Penurunan Kesadaran O:

TD:160/100 mmHg GCS: Delirium HR: 114x/menit RR: 20x/menit Temp: 37.2 C

A: Penurunan Kesadaran ec. Hiperglikemia Susp. HHS dd. KAD

P: Rehidrasi NaCl 20cc, 1 jam

pertama 1 jam kedua rehidrasi NaCl

500cc Pasang Kateter Urine Cek Kimia Darah tidak

tersedia Cek GDS/4 jam Saran: Pindah Rawat ke ICU O2 nasal kanul 2 lpm Glibenclamid stop insuline

sliding scale Insuline sliding scale:

<200: 0 u 200 – 250 : 15 u 250 – 300 : 10 u 300 – 350 : 15 u >350 : 20 u

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(02.00 WIB) ICU S: - O:

TD: 123/84 mmHg HR: 165 x/menit SpO2: 99% Urine Output: 20 cc GDS: 77 mg/dL

A: Susp. HHS

P: (dr. Ellidya, Sp.PD) Drip Dobutamine 1

Ampul dalam 100 cc NS 12 tpm maks. 20 tpm

IVFD: D5% 10 tpm O2 nasal kanul 2 lpm Insuline sliding scale

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(04.50 WIB) ICU S: - O:

HR: tidak teraba EKG: Ventricle

Takikardia GDS: 101 mg/dL

A: Cardiac Arrest + Susp. HHS

P: RJP 1 siklus Respon (+) Setelah RJP: HR: 64x/menit TD: 64/54 mmHg RR: 32 x/menit EKG: irama sinus, Tall T

wave, monitor bila terjadi VT berulang

Terapi: Dopamin 1 Amp.

(dobutamin kosong) dalam 100 cc NS 10 tpm

O2 nasal kanul 2 lpm Insuline sliding scale

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(06.50 WIB) ICU S: - O:

TD: 96/59 mmHg MAP: 65 mmHg

SpO2: 98% HR: 68 x/menit RR: 29 x/menit

A: Susp. HHS

P: Dopamine 1 Amp

dalam 100 cc NS 10 tpm

O2 nasal kanul 2 lpm

IVFD: D5% 20 tpm

Insuline sliding scale

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(9/12/2015) (08.00 WIB) ICU S: - O:

GCS: E1V1M1

TD: 138/79 mmHg HR: 90 x/menit RR: 29 x/menit SpO2: 96% GDS: 159 mg/dL Ur: 80 mg/dL

Cr: 2.3 mg/dL A: Susp. HHS dd.

KAD

P: IVFD: I NaCl 20 tpm/8

jam O2 nasal kanul 2 lpm Insuline sliding scale

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(12.00 WIB) ICUKeluarga Pasien menolak dirujuk ke Bengkulu. Keluarga pasien meminta pasien pulang. Pasien pulang atas permintaan keluarga.

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Review:Hyperglycemia Hyperosmolar State

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Diabetic Ketoacidosis (DKA) A state of absolute or relative insulin deficiency

aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone.

Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin deficiency/dependence

The presenting symptom for ~ 25% of Type I Diabetics.

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Diagnostic Criteria for DKA and HHSMild DKA Moderate DKA Severe DKA HHS

Plasma glucose (mg/dL)

> 250 > 250 > 250 > 600

Arterial pH 7.25-7.30 7.00-7.24 < 7.00 > 7.30

Sodium Bicarbonate (mEq/L)

15 – 18 10 - <15 < 10 > 15

Urine Ketones Positive Positive Positive Small

Serum Ketones Positive Positive Positive Small

Serum Osmolality (mOsm/kg)

Variable Variable Variable > 320

Anion Gap > 10 > 12 > 12 variable

Mental Status Alert Alert/Drowsy Stupor/Coma Stupor/Coma

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Causes of DKA/HHS Stressful precipitating event that results in increased

catecholamines, cortisol, glucagon. Infection (pneumonia, UTI) Alcohol, drugs Stroke Myocardial Infarction Pancreatitis Trauma Medications (steroids, thiazide diuretics) Non-compliance with insulin

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Pathophysiology of DKA

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Symptoms of DKA/HHS Polyuria Polydypsia Blurred vision Nausea/Vomiting Abdominal Pain Fatigue Confusion Obtundation

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Physical Examination in DKA Hypotension, tachycardia Kussmaul breathing (deep, labored breaths) Fruity odor to breath (due to acetone) Dry mucus membranes Confusion Abdominal tenderness

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Diagnostic Studies in DKA/HHS Chemistry

Glucose Bicarbonate Anion gap = (Na+) – (Cl- + HCO3

-) Frequently seen:

BUN/creatinine (dehydration) potassium sodium

Pseudohyponatremia: to correct, add 1.6 mEq of sodium to every 100mg/dL of glucose above normal

Serum acetones Positive in DKA

Urinalysis Ketones (for DKA); leukocyte esterase,

WBC (for UTI)

CBC Leukocytosis (possible

infection) Amylase/Lipase

To evaluate for pancreatitis BUT, DKA by itself can also

increase them! EKG

Evaluate for possible MI

Treatment of HHS Hydration!!!

Even more important than in DKA Find underlying cause and treat! Insulin drip

Should be started only once aggressive hydration has taken place.

Switch to subcutaneous regimen once glucose < 200 and patient eating.

Serial Electrolytes Potassium replacement.

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Possible Complications of DKA Hypophosphatemia

Occurs after aggressive hydration/treatment Monitor phosphorus and replete as needed to keep > 1

Cerebral edema Rare, but life threatening Usually in pediatric, adolescent patients Symptoms: Headache, altered mental status Treat with mannitol, hyperventilation

Myocardial infarction, DVT/PE, cardiac arythmias

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Portfolio Case Summary

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Patient suspected had Hyperglycemia Hyperosmolar State based on:

Anamnesis: Progressive unconscious state Uncontrolled diabetes mellitus He had no miction > 4hrs

Physical findings: Kussmaul’s type breathing Crackles on lung auscultation

Laboratory findings: Blood glucose: 474 mg/dL Leukocyte: 11.600 cell/mm3

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Therapy given to patient during hospitalised: Rehydration

Patient rehydrated by NS 200 cc in 1 hour 500 cc in next hour

Hyperglycemia therapy Patient given bolus insulin based on glucose sliding scale<200: 0 u200 – 250 : 15 u250 – 300 : 10 u300 – 350 : 15 u>350 : 20 u

Infection therapy Patient given antibiotic: ceftriaxone 1 gr per 12 hrs

intravenously

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References Soewondo, P. 2009. Ketoasidosis diabetik. In: Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiati

S. Buku Ajar Ilmu Penyakit Dalam. Edisi Kelima. Interna Publishing. 2009. Hal. 1906 – 1911 Kitbachi AE, Umpierrez GE, Miles JM, Fisher JN: Hyperglycemia crises in adult patients with diabetes.

Diabetes Care 2009; 32: 1335 – 1343 Goetara W, Budiyasa DGA. Penatalaksanaan ketoasidosis diabetik. Diakses dari: http://download.portalgaruda.org/article.php?article=13245&val=927 McNaughton CD, Wesley H, Solvis C. Diabetes care in the emergency departement: acute care of

diabetes patients. Clin Diab 2011;29:2 Soewondo P. Soegondo S, Suastika K, Pranoto A, Soeatmadji DW, Tjokroprawiro A. The Diabcare Asia

Study. 2008. Outcome on control and complications of type 2 diabetic patients in Indonesia. Diakses dari: http://mji.ui.ac.id/journal/index.php/mji/article/view/412

Soewondo, P. 2009. Ketoasidosis diabetik. In: Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiati S. Buku Ajar Ilmu Penyakit Dalam. Edisi Kelima. Interna Publishing. 2009. Hal. 1906 – 1911

Kitbachi AE, Umpierrez GE, Miles JM, Fisher JN: Hyperglycemia crises in adult patients with diabetes. Diabetes Care 2009; 32: 1335 – 1343

Goetara W, Budiyasa DGA. Penatalaksanaan ketoasidosis diabetik. Diakses dari: http://download.portalgaruda.org/article.php?article=13245&val=927 McNaughton CD, Wesley H, Solvis C. Diabetes care in the emergency departement: acute care of

diabetes patients. Clin Diab 2011;29:2 Soewondo P. Soegondo S, Suastika K, Pranoto A, Soeatmadji DW, Tjokroprawiro A. The Diabcare Asia

Study. 2008. Outcome on control and complications of type 2 diabetic patients in Indonesia. Diakses dari: http://mji.ui.ac.id/journal/index.php/mji/article/view/412