English Case Presantation To Whom

Respectfully ...............................

Hamdi

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Acute Renal Injury in A Boy with Diabetic Ketoacidosis

Introduction

Diabetes mellitus is a serious chronic disorder of childhood and represents a major

public health problem. Type 1 diabetes (T1D) is the predominant form of diabetes during

childhood and adolescence, accounting for about 90% of cases, although the growing epidemic

of obesity has been associated with an increasing number of cases of childhood-onset type 2

diabetes. The global incidence of type 1 diabetes is increasing worldwide, at an annual rate of

3-5%, particularly in children under the age of 5 years, and this trend leads to a significant

health burden. Recent studies have shown that in European countries childhood-onset T1D is

associated with three to four fold increased mortality when compared with the general

population. Similar data emerged from a long-term study of a young cohort with T1D in the USA,

where mortality was 7 times higher than in the non-diabetic population.

Diabetic ketoacidosis (DKA) occurs in 10 to 70% of children with T1D and has a

significant risk of mortality, mostly due to cerebral edema. Other potential complications of DKA

include hypokalemia, hypophosphatemia, hypoglycemia, intracerebral and peripheral venous

thrombosis, mucormycosis, rhabdomyolysis, acute pancreatitis, acute renal failure (ARF) and

sepsis. The development of ARF is a rare but potentially lethal disorder in children with DKA

with an estimated mortality of about 50%. The poor outcome of ARF associated with DKA

underlines the importance of earlyrecognition of ARF and early initiation of renal replacement

therapy.

The aim of this case report is to describe management DKA and ARF as complication of

DKA in children.

Case

A boy, J, 10 years and 7 months admitted to Pediatric ward M. Djamil hospital for 35 days

Chief complain: Unconciousness since 1 day before admitted.

Present Illness History:

Frequent feeling of thirst and hungry since 2 weeks ago. Frequent miction since 2 weeks ago,

especially at night, approximately every 1-2 hours. Loss of weight since 1 months ago. The last

weight was 36 kgs (1 month ago). Fatigue since 2 weeks ago. Fever since 5 days ago, not

high, intermittent, no shivering. Vomit 5 days ago, frequency about 10 times per day, about ¼ -

½ glass, contain food and drink, not projectile. Unconscious since 1 day ago. Perdarahan dari

NGT sejak 1 hari yang lalu, berwarna merah kecoklatan. Breathlessness since 8 hours ago, no

presence of wheezing, and not influenced by either weather or food. No headache, cold, cough,

seizure, numb at extremities, loss vision. No urinary since 8 hour ago. Defecation was normal.

Patients has been hospitalized at Bangko district hospital for 1 day, Random blood glucose was

368 gr/dl 324 gr/dl 349 gr/dl. Patient referred to M. Djamil hospital dengan suspek

Meningitis DD : Typhoid Encephalopaty, Malaria Serebral.

Past Illness History

Never suffered from disease like this before.

Family Illness History

Adik kakek pasien dari pihak bapak menderita DM

Pedigree

: Type 2 Diabetes mellitus

: Patient

History of Delivery, Immunization and Development

Patient was the first child, spontaneous delivery, aterm with birth weight 2900 grams and birth

length 50 cms, directly crying. Basic immunization was completed. History of growth and

development was normal. Hygiene and sanitation was not good.

Family and social economy history

His mother was 30 years old, graduated from junior high school, work as farmer. His father was

35 years old, graduated from elementary school, work as a farmer with income approximately

Rp. 1.500.000,00/month. Patient and his family live in their own home, a permanent house with

not good hygiene and sanitation.

Physical examination

Patient look severely ill with Glasgow Coma Scale (GCS): E1M2V1 = 4, blood pressure 60/20

mmHg, heart rate 156 times per minute, respiratory rate 60 times per minute, body temperature

37,7 oC, O2 saturation 98%, body weight 27 kgs, body height 127 cms, weight for age was

69,2%, height for age was 90%, weight for height was 103%, well nourished, there was no

anemic, no icteric, no edema and no cyanotic. Skin was cold. There was no regional lymph

enlargement. Head was round and symmetric, eyes were sunken, no eye drop, conjunctiva was

not anemic, sclera was not icteric, pupil isochors with diameter 2mm/2mm, light reflex was

positive normal. Ears was normal. There was nasal flare. Throat difficult to examine. Mucous in

mouth was dry, no oral trush. There was no neck rigidity, JVP 5-2 cmH2O. The chest was

symmetric, with Kusmaull respiration, there was epigastric retraction, heart: regular rhythm, no

murmur, lung: vesicular, no rales, no wheezing. There was no distension at abdominal, liver and

spleen was not palpable, turgor was slowly return, genitalia: puberty state A1P1G1. Extremities

was cold with bad perfusion, physiological reflex were positive normal, pathological reflex were

negative.

Laboratory finding:

Haemoglobin 11,6 gr%, leucocyte 28.800/mm3, differential count 0/1/3/74/20/2. Urinalisis:

albumin (+++), reduction (++), keton (++), leucocyte 1-2/LPB, erytocyte 0-1/LPB.

List of Problem

1. Shock

2. Metabolic Acidosis

3. Anuria

4. Gastrointestinal Bleeding

Working Diagnosis

1. Hipovolemic Shock, Differantial Diagnosis : Septic Shock

2. Suspected Diabetic ketoacidosis e.c Type 1 Diabetes Mellitus

3. Suspected Acute Kidney Injury

4. Gastro Intestinal Bleeding e.c suspected sepsis

Management

O2 2l/mnt,

IVFD RL 20 cc/kgBW in 15 minutes dalam 30 menit(2 lines)

Ceftriakson 1x 1,3 g IV

Omeprazol 1 x 15 mg IV

Follow up setelah 30 menit : syok belum teratasi dilanjutkan dengan pemberian cairan infus

RL 20 cc/kgBB dalam 30 menit.

Follow up setelah 60 menit : syok masih belum teratasi dilanjutkan dengan pemberian

cairan infus RL 20 cc/kgBB/30 menit

Follow up setelah 90 menit : syok masih belum teratasi dilanjutkan dengan infus RL 10

cc/kgBB/jam dan pemberian Dopamin dosis 5 microgram/kgBB/menit yang dinaikkan secara

bertahap setiap 15 menit sampai syok teratasi.

Syok teratasi setelah pemberian dopamin dosis 7,5 microgram/kgBB/menit

Fluid requirements:

Body weight : 27 kg

1. Degree of dehydration = severe (9%)

2. Fluid deficit = 9% x 27 x 1000 = 2430 cc

3. Concomitan requirements for 48 hours = 1640x2=3280 cc

4. Total 48 hours fluid = 3195+3620= 6815 cc

5. Cairan total yang akan diberikan selama 48 jam - cairan yang telah diberikan = 5710

- 1750 = 3960 = 82,5 cc/jam

6. Pemberian insulin regular drip = 0,1 iu/kgBB/jam = 0,5 cc insulin dalam 50 cc NaCl

0,9 % dengan kecepatan 1 ml/kgBB/jam --> 2,7 cc/jam

7. Kebutuhan cairan perjam untuk NaCl 0,9% = 82,5 - 2,7 = 79 cc/jam

Planning: Blood gas analysis (BGA), electrolyte, Random blood glucose (RBG) every 1

hour, and keton urin every 2 hours. Blood culture, HbA1C, C-peptide, fluid balance, consult

to Eye departement

Laboratorium

Blood Gas Analysis : pH : 7,01; pCO2: 10 mmHg, pO2: 157 mmHg, HCO3-: - , BE: -, SO2: -,

impression severe metabolic acidosis, we give sodium bicarbonate Random Blood Glucose

1141 mg/dl (hyperglycemia), Sodium 136 mmol/L, Potassium 3,2 mmol/L, Calsium 9,7 mmol/L,

ureum 215 mg/dl, kreatinin 4,5 mg/dl. PT 10,3, APTT 40,5. Impression : Increase of ureum and

cratinine with LFG 15,5% (failure: criteria RIFLE)

2 hour after admission (10.00)

Still unconciouss GCS E1M3V1=5, his breathlessness was decrease, without fever, cyanotic or

seizure, Buang air kecil belum ada. Patient look severely ill with heart rate 120 times/minute,

respiratory rate 34 times/minute, temperature 37 oC, blood pressure 100/70 mmHg, pupil was

isochor, diameter 2 mm, light reflex was +/+ normal, there was no nasal flare. There was no

nuchal rigidity, chest and stomach was normal, extremities was warm with good perfusion. The

treatment with oxygen 2 L/minute, IVFD NaCl 0,9% + Kcl 10 Meq/500 cc --> 34

drop/sec( macrodrop), fasting temporary, and insulin intravenous insulin. Blood glucose

revealed high, hasil AGD ulangan : pH :6,95; pCO2: 13 mmHg, pO2: 132 mmHg, HCO3-: < 3 ,

BE: -, SO2: -, impression severe metabolic acidosis, we give sodium bicarbonate. Fluid

challenge with Furosemid 1 mg/kgBB, naikkan dosis insulin 0,15 iu./kgBB/jam

5 hour after admission (13.00)

Patient still unconscious and had no fever or breathlessness. No urinary. Patient look severely ill

with GCS E1M3V1=5, heart rate 125 times/minute, respiratory rate 30 times/minute, temperature

37 oC, blood pressure 100/70 mmHg, pupil was isochor, diameter 3 mm, light reflex was +/+

normal, there was no nasal flare, chest and stomach was normal, extremities was warm with

good perfusion. We give oxygen 1 L/minute, fasting temporary, and continue insulin

intravenous. Dopamin 5 microgram/kgBB/menit. Blood glucose was 799 mg/dl. Blood gas

analysis was: pH: 7,21; pCO2: 27 mmHg; pO2: 133 mmHg; HCO3-: 10 mmol/L; BE: -

15,7mmol/L; SO2: 60% ( monitor 100%), it is a metabolic acydosis ( perbaikan dari

sebelumnya).

(2nd day of hospitalization)

Patient still unconcious, no fever, no breathlessness, there was no cyanotic and no seizure.

BGA about 300 - 400 mg/dl. Patient look severely ill, with GCS E2M3V2=7, heart rate 120

times/minute, respiratory rate 30 times/minute, temperature 37 oC, blood pressure 100/70

mmHg, pupil were isochor, diameter 2 mm, light reflex was +/+ normal, there was nasal flare,

chest and stomach was normal, extremities was warm and urination 0,3 cc.bw/hours. It is an

anuria acute kidney injury caused by DKA, continued the teraphy and planned to check the

RBG, renal and liver function, Brain CT Scan

Laboratory result:

RBG 220 mg/dl, ureum 285 mg/dl, kreatinin 7,2 mg/dl with LFG 9,7% (failure: criteria RIFLE).

Na: 147mmol/l, K: 3,3 mmol/l. SGOT 25 IU, SGPT 10 IU we give oksigen 1 l/1nasal, IVFD

dextrose 10%+KCL 20 meq/kolf. We plan to do hemodialisis, Urology ultrasonography.

Hemodialisis belum dapat dilakukan karena keterbatasan alat, direncanakan CAPD. Hasil CT

scan : tak tampak kelainan pada CT scan.

( 3rd day of hospitalization)

Patient still unconcious, no fever, no breathlessness, there was no cyanotic and no seizure.

BGA about 300 - 400 mg/dl. Patient look severely ill, with GCS E2M3V2=7, heart rate 120

times/minute, respiratory rate 30 times/minute, temperature 37 oC, blood pressure 110/70

mmHg, pupil were isochor, diameter 2 mm, light reflex was +/+ normal, there was nasal flare,

chest and stomach was normal, extremities was warm and urination 0,3 cc.bw/hours. Random

blood glucose was between 93 to 267 mg/dl.

(4th day of hospitalization)

Patient still unconcious, fever, no breathlessness, there was no cyanotic and no seizure.

Patient look severely ill, with GCS E2M3V2=7, heart rate 120 times/minute, respiratory rate 30

times/minute, temperature 38,5oC, blood pressure 110/70 mmHg, pupil were isochor, diameter 2

mm, light reflex was +/+ normal, there was nasal flare, chest and stomach was normal,

extremities was warm and urination 2,7cc.bw/hours. Random blood glucose was between 103

- 208 mg/dl. Ureum 285 mg/dl and kreatinin 7,8 mg/dl , LFG was 8,9% (failure: RIFLE criteria).

Therapy : O2 1l/minute, IVFD D12,5% 16 gtt/mnt(macro), Insulin drip 0,05 IU/kgBW = 1,3

cc/hour, Meropenem 1 x 1 gr, Furosemid 1x 27 mg, Omeprazol 1 x 15 mg. Plan : CAPD

(5th day of hospitalization)

Patient still unconcious, fever, no breathlessness, there was no cyanotic and no seizure.

Patient look severely ill, with GCS E2M3V2=7, heart rate 120 times/minute, respiratory rate 30

times/minute, temperature 38,5oC, blood pressure 110/70 mmHg, pupil were isochor, diameter 2

mm, light reflex was +/+ normal, there was nasal flare, chest and stomach was normal,

extremities was warm and urination 3,2.bw/hours. Random blood glucose was between 103 -

208 mg/dl. Ureum 336 mg/dl and kreatinin 6,7mg/dl (failure: RIFLE criteria). Therapy : O2

1l/minute, IVFD D12,5% 16 gtt/mnt(macro), Insulin drip 0,05 IU/kgBW = 1,3 cc/hour,

Meropenem 1 x 1 gr, Furosemid 1x 27 mg, Omeprazol 1 x 15 mg.

(6th - 7th day of hospitalization)

Patient still unconcious, no fever, no breathlessness, there was no cyanotic and no seizure.

Patient look severely ill, with GCS E2M3V2=7, heart rate 124 times/minute, respiratory rate 34

times/minute, temperature 36,5oC, blood pressure 110/70 mmHg, pupil were isochor, diameter 2

mm, light reflex was +/+ normal, there was nasal flare, chest and stomach was normal,

extremities was warm and urination 2,7 - 3 cc.bw/hours. Random blood glucose was between

103 - 208 mg/dl. Ureum 336 mg/dl and kreatinin 6,7mg/dl (failure: RIFLE criteria). Therapy :

O2 1l/minute, IVFD D12,5% 16 gtt/mnt(macro), Insulin drip 0,05 IU/kgBW = 1,3 cc/hour,

Meropenem 1 x 1 gr, Furosemid 1x 27 mg, Omeprazol 1 x 15 mg.

(8th day of hospitalization)

Patient still unconcious, no fever, no breathlessness, there was no cyanotic and no seizure.

Patient look severely ill, with GCS E2M3V2=7, heart rate 120times/minute, respiratory rate 30

times/minute, temperature 37,5oC, blood pressure 110/70 mmHg, pupil were isochor, diameter 2

mm, light reflex was +/+ normal, there was nasal flare, chest and stomach was normal,

extremities was warm and urination 2,7 - 3 cc.bw/hours. Random blood glucose was between

150 - 235 mg/dl. Ureum 275 mg/dl and kreatinin 7,6 mg/dl (failure: RIFLE criteria). Therapy :

O2 1l/minute, IVFD D12,5% 16 gtt/mnt(macro), Insulin drip 0,05 IU/kgBW = 1,3 cc/hour,

Meropenem 1 x 1 gr, Furosemid 1x 27 mg, Omeprazol 1 x 15 mg. Plan : CAPD

(10th day of hospitalization)

CAPD sudah dilakukan, demam, sesak nafas, kejang tidak ada, perdarahan tidak ada, anak

sudah diberi minum MC 6 x 50 cc/NGT, CAPD lancar. Buang air kecil 1,9 cc/kgBB/jam. GDR

berkisar 150 - 200 mg/dl.

Patient look severely ill, with GCS E4M5V3=12, heart rate 120 times/minute, respiratory rate 30

times/minute, temperature 36,5oC, blood pressure 110/70 mmHg, pupil were isochor, diameter 2

mm, light reflex was +/+ normal, there was nasal flare, chest and stomach was normal,

extremities was warm. Ureum 262 mg/dl , Kreatinin 5,8 mg/dl. Random blood glucose was

between 150 - 235 mg/dl.

Therapy : MC 6 x 50 cc/NGT , IVFD D12,5% 14 gtt/mnt(macro), aminofusin paed 5% 500cc/

day, Insulin drip 0,05 IU/kgBW = 1,3 cc/hour, Meropenem 1 x 1 gr, Omeprazol 1 x 15 mg.

(11th day of hospitalization)

Anak demam, NGT mengalir cairan coklat kehitaman, tidak ada muntah dan kejang. Buang air

kecil 1,9 cc/kgBB/jam

Patient look severely ill, with GCS E3M5V2=10, heart rate 130 times/minute, respiratory rate 30

times/minute, temperature 38,5oC, blood pressure 110/70 mmHg, pupil were isochor, diameter 2

mm, light reflex was +/+ normal, there was nasal flare, chest and stomach was normal,

extremities was warm. Hb 8,7 g/dl, Leukosit 25900/mm3 , APTT memanjang 2,5 kali. Kesan :

perdarahan saluran cerna e.c Sepsis. Ureum 202 mg/dl, Kreatinin 3,4 mg/dl. Random blood

glucose was between 150 - 250 mg/dl.

Therapy : Fasting temporary, IVFD D12,5% 16 gtt/mnt(macro), aminofusin paed 5% 500cc/ day,

Insulin drip 0,05 IU/kgBW = 1,3 cc/hour, Meropenem 1 x 1 gr, Omeprazol 1 x 15 mg. FFP

Transfusion 3 x 250 cc. CAPD/6 jam.

(14th day of hospitalization)

Anak tidak demam, NGT jernih, tidak ada muntah, kejang. Buang air kecil cukup. Buang air

besar biasa, CAPD lancar, GDR normal.

Patient look severely ill, with GCS E4M5V3=13, heart rate 113 times/minute, respiratory rate 30

times/minute, temperature 37,4oC, blood pressure 110/70 mmHg, pupil were isochor, diameter 2

mm, light reflex was +/+ normal, there was nasal flare, chest and stomach was normal,

extremities was warm. Ureum 83 mg/dl, kreatinin 1 mg/dl. Random blood glucose was between

150 - 250 mg/dl.

Therapy : MC 6 x 50 cc/NGT, IVFD D12,5% 14 gtt/mnt(macro), aminofusin paed 5% 500cc/

day, Insulin drip 0,05 IU/kgBW = 1,3 cc/hour, Meropenem 1 x 1 gr, Omeprazol 1 x 15 mg.

CAPD/6 jam.

(17th day of hospitalization)

Anak sadar penuh, tidak ada demam, muntah, kejang dan perdarahan. Buang air kecil cukup.

Buang air besar biasa. Anak dipindahrawatkan dari HCU ke ruangan non infeksi.

Patient look severely ill, conciusnes, heart rate 110 times/minute, respiratory rate was 26

times/minute, temperature 37,2 oC, blood pressure 100/60 mmHg. Pupil was isochor, diameter 2

mm, light reflex was +/+, there was nasal flare, chest and stomach was normal. Extremities was

warm with good perfusion. It is an improvement than before. Random blood glucose was

between 93 to 267 mg/dl. Ureum 31 mg/dl, kreatinin 0,1 mg/dl.

Therapy :

MC DM Makan Pagi 320 kkal, snack pagi 160 kkal, makan siang 480 kkal, snack siang 160

kkal, makan malam 360 kkal, snack malam 160 kkal. Antibiotik meropenem 3 x 1 gr IV. Insulin

Levemir 8-8, Noverapid 5-7-5. Rencana : Buka CAPD

(21st day of hospitalization)

Anak direncanakan buka CAPD, pemberian insulin subkutan dihentikan sementara, diberikan

drip insulin. Intake masuk per NGT, muntah tidak ada, demam tidak ada.

(22th day of hospitalization)

CAPD sudah dibuka, anak sadar penuh, tidak ada demam, muntah, kejang dan perdarahan.

Buang air kecil cukup. Buang air besar biasa. Anak dipindahrawatkan dari HCU ke ruangan non

infeksi.

Conciusnes, heart rate 110 times/minute, respiratory rate was 26 times/minute, temperature

37,2 oC, blood pressure 100/60 mmHg. Pupil was isochor, diameter 2 mm, light reflex was +/+,

there was nasal flare, chest and stomach was normal. Extremities was warm with good

perfusion. It is an improvement than before. Random blood glucose was between 93 to 267

mg/dl.

Therapy :

MC DM Makan Pagi 320 kkal, snack pagi 160 kkal, makan siang 480 kkal, snack siang 160

kkal, makan malam 360 kkal, snack malam 160 kkal. Antibiotik meropenem 3 x 1 gr IV. Insulin

Levemir 8-8, Noverapid 5-7-5.

(25th day of hospitalization)

Anak sadar penuh, tidak ada demam, muntah, kejang dan perdarahan. Buang air kecil cukup.

Buang air besar biasa.

Conciusnes, heart rate 114 times/minute, respiratory rate was 26 times/minute, temperature

37,2 oC, blood pressure 100/60 mmHg. Pupil was isochor, diameter 2 mm, light reflex was +/+,

there was nasal flare, chest and stomach was normal. Extremities was warm with good

perfusion. It is an improvement than before.

Therapy : MB diet DM 2000 kkal. Makan pagi 400 kkal, snack pagi 200 kkal, makan siang 600

kkal, snack sore 200 kkal, makan malam 400 kkal, snack malam 200 kkal. Levemir 5-2.

Noverapid 2-2-2. Total insulin 0,5 iu/kgBB/hari.

(35th day of hospitalization)

Pasien diperbolehkan pulang.

Literature Review

Diabetic ketoacidosis is an acute and life-threatening complication of diabetes mellitus and

consist of the biochemical triad of hyperglycemia, ketonemia and metabolic acidosis. Even in

reference centers, 15 to 67% of diabetic patients still present DKA as the first manifestation of

type 1 diabetes, mainly in children under 5 years old and in population with difficult access to

health services for socioeconomic reasons. In Brazil, recent studies have shown that DKA was

present in 32,8 to 41% of the patient at the time of diagnosis of type 1 DM, in agreement with

international data.

DKA is the most frequent cause of hospitalization and mortality among type 1 diabetes

children and adolescent, and it accounts for approximately 50% of all deaths of DM individuals

up to 24 years of age. In developed countries, DKA mortality rate is 0,15% to 5% and it is mainly

due to cerebral edema, occurring in about 1% of the cases.

Cerebral edema is a life threatening complication of diabetic ketoacidosis (DKA), other

complications include dyselectrolytemia, acute respiratory distress syndrome (ARDS),

pulmonary edema and renal failure. Chronic renal failure due to diabetic nephropathy and its

presentation with DKA is encountered in adults. But children with new onset diabetes mellitus

(DM) or known diabetic children presenting with acute renal failure (ARF) is rare. Literature

reveals few case reports of DKA with renal failure. Reported mortality in ARF complicating DKA

is about 50%

The diabetic patient is particularly susceptible to the development of acute renal failure.

Hypovolaemia and sepsis, with a background of chronic renal disease predispose to this

important complication. The importance of acute renal failure lies not so much in its frequency

as in the high mortality and morbidity when it complicates the course of illness in diabetics.

Acute kidney injury (AKI) formerly known as acute renal failure (ARF) is a clinical

syndrome that has been known by about twenty-five different nomenclature over the years. It

evolved from the 18th century when it was first known as “ischuria renalis” (“ischuria” meaning

suppression of urinary output) to the current terminology “acute kidney injury” in the 21st

century. Acute kidney injury has also been defined in over thirtyfive different ways in the last few

centuries. It is widely defined as a clinical syndrome characterised by a sudden deterioration in

renal function resulting in an inability of the kidneys to maintain fluid and electrolyte

homeostasis. It has also been defined as onset of reduced kidney function manifested by

increased serum creatinine or a reduction in urine output.

RIFLE is a mnemonic for level of severity & outcome. There are 3 levels of severity;

Risk, Injury and Failure and 2 outcomes measures; Loss of renal fuction and End -stage renal

disease (ESRD). The pRIFLE a modified form for paediatric use can be seen in Table 2.

Hyperglycaemic hyperosmolar non-ketotic coma

Hyperglycaemic hyperosmolar non-ketotic coma is a well-recognized clinical entity

which under certain circumstances can lead to acute renal failure. It accounts for between 10

to 33 % of "diabetic comas" , and typically occurs in patients over the age of 55, with no

previous history of diabetes. Those patients known to have diabetes are almost invariably

non-insulin dependent. West Indians appear to have an increased incidence of

h yperglycaemic hyperosmolar coma, which tends to occur at a younger age. Symptoms

develop over several days to weeks with increasing thirst, polyuria, and drowsiness. On

admission the blood glucose is usually very high (>50 mmol/l), the majority are severely

dehydrated, and up to 30% may be hypotensive. Neurological abnormalities are common and

often result in the erroneous diagnosis of cerebrovascular accident.

The mortality from hyperglycemic hyperosmolar non-ketotic coma is high between 30-

60% in most large series. The advanced age of the patients, a delay in making the diagnosis,

and the presence of serious underlying conditions (pancreatitis, chronic renal impairment,

myocardial infarction, and sepsis), all contribute to this high mortality rate. However,

therapeutic error is also important, especially in the development of acute renal failure, and

when early death occurs from hypovolaemic shock.

Acute renal failure complicating hyperglycaemic hyperosmolar coma may arise as a

result of the severe dehydration and hypovolaemia, or as a consequence of inappropriate or

inadequate treatment. Preexisting renal impairment is common and predisposes to the

development of acute renal failure.

The treatment of hyperglycaemic hyper osmolar non-ketotic coma is fraught with

difficulties and may itself lead to cardiovascular collapse and acute renal failure. Appropriate

fluid replacement is of vital importance. These patients are severely dehydrated, and yet their

increased age, the likelihood of cardiac disease and impaired renal function makes rapid fluid

replacement hazardous. It is essential to monitor central venous pressure, and in some cases,

pulmonary artery catheterization may be necessary.

The type of fluid infused remains controversial. Several authorities recommend

hypotonic saline (0.45% ) in all cases, whereas others recommend isotonic saline (0.9%). There

is a strong case for initiating therapy with isotonic saline. Even though the patient may be

severely hypertonic, hypovolaemic shock is the immediate threat to life. Hypotonic saline may

not restore intravascular volume rapidly enough to avert irreversible organ damage, since most

of the fluid infused will pass into the intracellular space. Whatever the type of fluid infused (and

it may be that the rate of infusion is more important), it is essential to restore blood pressure,

tissue perfusion, and urine output, and so prevent cardiovascular collapse and acute renal

failure.

Insulin treatment is far less important in the management of hyperglycaemic hyper

osmolar coma than either fluid replacement or the treatment of underlying conditions, and

provides another source of error which may lead to acute renal failure. Under normal

circumstances, only small doses of insulin are required (2 - 6 U/h), large doses being not only

unnecessary but also dangerous. Hypotension early in the course of treatment with large doses

of insulin has been reported by several investigators and again this seems to be related to a

rapid reduction in plasma osmolality.

Diabetic ketoacidosis

Diabetic ketoacidosis is a much more common cause of metabolic decompensation in

the diabetic than hyperglycaemic hyperosmolar non-ketotic 'coma'. Fortunately the mortality is

considerably lower, ranging from 2-18% with the majority of cases making an uncomplicated

recovery. Despite this, it is a critical condition since it occurs most commonly in young insulin

dependent diabetics, and is the commonest cause of death in these patients. The major causes

of death are irreversible acute circulatory failure, overwhelming infection and myocardial

infarction. Acute renal failure, although a rare complication of diabetic ketoacidosis, contributes

to this mortality.

The severe dehydration of diabetic ketoacidosis results from the osmotic diuresis

secondary to hyperglycaemia, and fluid deficits average 5 to 7 L. The development of ketosis

causes patients to present sooner than those with hyperglycaemic hyperosmolar 'coma', and

thus dehydration is less severe, and hypotension less common. Nevertheless hypotension does

occur and may lead to acute renal failure. Keller et al. in their review of diabetic 'comas' noted

that hypotension and oliguria were common especially in those that died.

The management of diabetic ketoacidosis is usually straightforward and has been

reviewed by several authors. The prevention of acute renal failure lies in the prompt initiation of

treatment and the adequate replacement of fluid deficits with isotonic saline. Similar arguments

for the use of isotonic saline prevail as for hyperglycaemic hyperosmolar 'coma'. Colloid may be

used in the treatment of severe hypotension, since hyperviscosity is less severe than in

hyperglycaemic hyperosmolar coma. If acute renal failure should develop, dialysis must be

initiated early rather than late, since hyperglycaemia, hyperkalaemia and acidosis are difficult to

manage in the oliguric patient.

Septicaemia

Septicaemia is an important cause of acute renal failure and may account for up to 20%

of all cases of acute renal failure. Diabetics are particularly prone to septicaemia often in

association with urinary tract infections, and may develop acute renal failure as a result. The

mechanisms responsible are uncertain, but are thought to include severe hypotension and intra-

vascular coagulation.

The prevention of these problems in the diabetic depends on early diagnosis and

treatment with appropriate antimicrobials. It is important to remember that the diabetic when

septic commonly presents in ketoacidosis or hyperosmolar 'coma', and such patients should be

carefuly screened for infection.

Management of the diabetic with acute renal failure

The management of the diabetic with acute renal failure is in essence the same as for

non-diabetics but may pose additional problems related to the diabetic state. These relate to

problems of blood glucose control and dialysis in the uraemic diabetic.

Metabolic control

Although uraemia is commonly associated with carbohydrate intolerance,

hyopglycaemia and reduced daily insulin requirements are frequently observed in diabetic

patients with chronic renal failure. Anorexia and vomiting reduce carbohydrate intake. Renal

metabolism of insulin may be decreased by 50-77% resulting in higher levels of plasma insulin

[46]. In addition, urinary excretion of insulin is reducedas glomerular filtration decreases.

Insulin requirements in diabetic patients who develop acute renal failure are

considerably reduced. Thus, hypoglycaemia may be a problem; carbohydrate intake should be

increased and attempts made to minimize vomiting.

Potassium

Hyperkalaemia is a common problem in acute renal failure especially in hypercatabolic

patients and in diabetics the situation is complex. In both ketoacidosis and hyperosmolar 'coma'

total body potassium is reduced but in the presence of acute renal failure great care should be

taken over potassium supplementation. In addition the use of insulin and glucose infusions will

cause the serum potassium to fall, making regular measurement of the serum potassium

essential.

Peritoneal dialysis

The use of peritoneal dialysis to treat renal failure in diabetics has increased

considerably over the past few years. It may be used successfully to treat acute renal failure,

and has certain advantages for the diabetic compared to haemodialysis. There are no access

problems, and rapid fluid shifts do not occur. It is simple to use and offers the possibility of good

metabolic control by the administration of insulin via the intraperitoneal route. However, in the

highly catabolic patients haemodialysis or haemofiltration is the treatment of choice.

Case analysis

The patient described in this case report had severe acute oliguric acute renal failure associated

with diabetic ketoacidosis. DKA is defined by the American Diabetes Association, the European

Society for Paediatric Endocrinology, and the Pediatric Endocrine Society as hyperglycemia

(plasma glucose > 200 mg/dL or approximately 11 mmol/L) and venous pH < 7.3 and/or

bicarbonate < 15 mmol/L. It was suitable with patient, when he came, Blood Gas Analysis : pH :

7,01; HCO3 wasn’t read, Random Blood Glucose 1141 mg/dl (hyperglycemia).