ASUHAN KEPERAWATAN

Diabetic Ketoacidosis
Hyperglycemic Hyperosmolar State

1
 DKA Hospital Discharges in the US
Growth in Incidence 1988-2009
160
1988: 80,000 discharges 2009: 140,000 discharges
140
Number (thousands)

120
100
80
60
40
20
0

CDC. Diabetes data and trends. Hospitalization: DKA. Available from:

[Link]
2
 DKA Mortality in the US
Decline in Incidence 1988-2009
3500 1988: 3189 deaths 2009: 2417 deaths
3000

2500
Number

2000

1500

1000

500

CDC. Diabetes data and trends. DKA mortality. Available from:

[Link]
3
 Death Rates for Hyperglycemic Crises as
Underlying Cause
Rate per 100,000 Persons with Diabetes
By Age, United States, 2009
25
20.7
20
Deaths per 100,000

14.8
15
11.1
10
6.5
5

0
0-44 45-64 65-71 ≥75
Age (years)

CDC. Diabetes complications. Mortality due to hyperglycemic crises. Available from:

[Link]
4
OVERVIEW

5
 Characteristics of DKA and HHS

Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar State (HHS)

Absolute (or near-absolute) insulin Severe relative insulin deficiency, resulting

deficiency, resulting in in
• Severe hyperglycemia • Profound hyperglycemia and
• Ketone body production hyperosmolality (from urinary free
• Systemic acidosis water losses)
• No significant ketone production or
acidosis
Develops over hours to 1-2 days Develops over days to weeks
Most common in type 1 diabetes, but Typically presents in type 2 or previously
increasingly seen in type 2 diabetes unrecognized diabetes
Infeksi, stress, autoimune disorder, Intake Kh Berlebih + Terapi Menurun,
genetic predisposition, unknow Inadequate Insulin, Metabolic Syndrom,
environment Insulin Resisten, Recent Acute Illness
6
 Definition of Diabetic Ketoacidosis*

Acidosis

*
Ketosis
Hyperglycemia
Adapted from Kitabchi AE, Fisher JN. Diabetes Mellitus. In: Glew RA, Peters SP, ed. Clinical
Studies in Medical Biochemistry. New York, NY: Oxford University Press; 1987:105.
7
 MANIFESTASI DKA

GEJALA HASIL LAB

• HAUS dan Polyuria • HYPERGLIKEMIA
• Takikardia dan hipotensi • HYPONATREMIA
• Penurunan turgor kulit • NORMAL/>> SERUM
• Membran mukasa kering POTASIUM
• Pernafasan kusmaul • Mg, Ca, Pospat (menurun)
• Tanda infeksi (demam) • Hyperosmolar
• Penurunan status mental • Asidosis metabolik
• Keton naik

8
 Lab Findings in DKA

• Hyperglycemia
• Usually >250 mg/dL
• Lower blood glucose values possible, especially under
metabolically stressful conditions (eg, prolonged fasting,
carbohydrate avoidance, extreme sports/physical exertion,
myocardial infarction, stroke, severe infection, surgery)
• Increased blood and urine ketones
• High -hydroxybutyrate
• High anion gap
• Low arterial pH
• Low PCO2 (respiratory compensation)

Handelsman Y, et al. Endocr Pract. 2016;22:753-762.

9
Causes of Morbidity and Mortality in DKA

• Shock • Acute renal failure

• Hypokalemia during • Acute respiratory
treatment distress syndrome
• Hypoglycemia during • Vascular thrombosis
treatment • Precipitating illness,
• Cerebral edema including MI, stroke,
during treatment sepsis, pancreatitis,
• Hypophosphatemia pneumonia

10
 Hyperosmolar Nonketotik Hyperglicemia
Syndrom*
hiperosmolar

*
dehidrasi
Hyperglycemia
Adapted from Kitabchi AE, Fisher JN. Diabetes Mellitus. In: Glew RA, Peters SP, ed. Clinical
Studies in Medical Biochemistry. New York, NY: Oxford University Press; 1987:105.
11
 MANIFESTASI HONK

GEJALA HASIL LAB

• Penurunan kesadaran • HYPERGLIKEMIA
• Dehidrasi berat • HYPONATREMIA
• Disfungsi renal • NORMAL/>> SERUM
POTASIUM
• Mg, Ca, Pospat (menurun)
• Hyperosmolar lebih terlihat

12
PATHOGENESIS AND
PATHOPHYSIOLOGY
13
Diabetic Ketoacidosis: Pathophysiology

Unchecked gluconeogenesis  Hyperglycemia

Osmotic diuresis  Dehydration

Unchecked ketogenesis  Ketosis

Dissociation of ketone bodies into Anion-gap metabolic


hydrogen ion and anions acidosis

Often a precipitating event is identified

(infection, lack of insulin administration)

14
 Pathogenesis of Hyperglycemic Crises
DKA HHS

Hyperglycemia Dehydration Lipolysis-

osmotic diuresis
Increased FFA

Increased
glucose
Increased
production
ketogenesis
Insulin Counterregulatory
Deficiency Hormones

Decreased
glucose Metabolic
uptake acidosis
Electrolyte Hypertonicity
abnormalities
Umpierrez G, Korytkowski M. Nat Rev Endocrinol. 2016;12:222-232.
15
 Insulin Deficiency

Hyperglycemia

Hyper-
osmolality
Glycosuria

Δ MS
Dehydration

Electrolyte
Renal Failure Losses

Shock CV
Collapse 16
Insulin Deficiency

Lipolysis

FFAs

Ketones

Acidosis

CV
Collapse 17
 Insulin Deficiency

Hyperglycemia Lipolysis

Hyper-
osmolality
Glycosuria FFAs

Δ MS Ketones
Dehydration
Acidosis
Electrolyte
Renal Failure Losses

Shock CV
Collapse 18
 Hyperosmolar Hyperglycemic State:
Pathophysiology

Unchecked gluconeogenesis  Hyperglycemia

Osmotic diuresis  Dehydration

• Presents commonly with renal failure

• Insufficient insulin for prevention of hyperglycemia but
sufficient insulin for suppression of lipolysis and ketogenesis
• Absence of significant acidosis
• Often identifiable precipitating event (infection, MI)

19
 Diabetic Hyperglycemic Crises

Diabetic Ketoacidosis Hyperglycemic Hyperosmolar State

(DKA) (HHS)

Younger, type 1 diabetes Older, type 2 diabetes

No hyperosmolality Hyperosmolality

Volume depletion Volume depletion

Electrolyte disturbances Electrolyte disturbances

Acidosis No acidosis

20
PATIENT PRESENTATION

21
 Electrolyte and Fluid Deficits in
DKA and HHS
Parameter DKA* HHS*

Water, mL/kg 100 (7 L) 100-200 (10.5 L)

Sodium, mmol/kg 7-10 (490-700) 5-13 (350-910)

Potassium, mmol/kg 3-5 (210-300) 5-15 (350-1050)

Chloride, mmol/kg 3-5 (210-350) 3-7 (210-490)

Phosphate, mmol/kg 1-1.5 (70-105) 1-2 (70-140)

Magnesium, mmol/kg 1-2 (70-140) 1-2 (70-140)

Calcium, mmol/kg 1-2 (70-140) 1-2 (70-140)

* Values (in parentheses) are in mmol unless stated otherwise and refer to the total
body deficit for a 70 kg patient.
Chaisson JL, et al. CMAJ. 2003;168:859-866.
22
 Initial Laboratory Evaluation of
Hyperglycemic Emergencies
• Comprehensive metabolic profile
• Serum osmolality
• Serum and urine ketones
• Arterial blood gases
• Lactate (?)
• CBC
• Urinalysis
• ECG
• Blood cultures (?)
23
 Laboratory Diagnostic Criteria of
DKA and HHS
Parameter Normal range DKA HHS
Plasma glucose, mg/dL 76-115 ≥250* ≥600
Arterial pH† 7.35-7.45 ≤7.30 >7.30
≥31 (children)
-Hydroxybutyrate, mg/dL 4.2-5.2
≥40 (adults)
Serum bicarbonate, mmol/L‡ 22-28 ≤18 >15
Effective serum osmolality, mmol/kg 275-295 ≤320 >320
Anion gap,§ mmol/L <10 >10 Variable
Serum ketones¶ Negative Positive None or trace
Urine ketones‡ Negative Moderate to high None or trace
*May occur at lower glucose values, especially under physiologically stressful conditions.
† If venous pH is used, a correction of 0.03 must be made.
‡ Suggestive but not diagnostic of DKA.
§ Calculation: (Na+) – [Cl- + HCO - (mEq/L)].
3
¶ Nitroprusside reaction method.

Chaisson JL, et al. CMAJ. 2003;168:859-866. Handelsman Y, et al. Endocr Pract. 2016;22:753-762. Haw SJ, et al.
In: Managing Diabetes and Hyperglycemia in the Hospital Setting: A Clinician’s Guide. Draznin B, ed. Alexandria,
VA: American Diabetes Association; 2016;284-297.
24
 ADA Diagnostic Criteria for
DKA and HHS
DKA
Parameter Mild Moderate Severe HHS
Plasma glucose, mg/dL >250 >250 >250 >600
Arterial pH 7.25-7.3 7.0-7.24 <7.0 >7.30
Serum bicarbonate, mmol/L 15-18 10 to <15 <10 >15
Serum ketones† Positive Positive Positive Small
Urine ketones† Positive Positive Positive Small
Effective serum osmolality,*
Variable Variable Variable >320
mOsm/kg
Alteration in sensoria or mental
Alert Alert/drowsy Stupor/coma Stupor/coma
obtundation
*Calculation: 2[measured Na+ (mEq/L)] + glucose (mg/dL)/18.
† Nitroprusside reaction method.

ADA. Diabetes Care. 2003;26:S109-S117.

25
 DKA and Abdominal Pain

Presenting With Presenting Without

Abdominal Pain Abdominal Pain
Characteristic (n=86) (n=103)
Age, years 37 ± 1† 41 ± 2
Male gender, n 47 64
History of alcohol use, % 51* 24
History of cocaine use 13‡ 2
Blood glucose, mg/dL 596 586
Bicarbonate, mmol/L 9 ± 1* 15 ± 1
Ph 7.12 ± 0.02* 7.24 ± 0.09
Sodium, mmol/L 133 ± 1 133 ± 1
Serum osmolality, mmol/L 307 ± 2 307 ± 2

*P<0.05. †P<0.01. ‡P<0.0001.

Umpierrez G, Freire AX. J Crit Care. 2002;17:63-67.
 Clinical Characteristics of DKA Patients
Presenting With Abdominal Pain
With abdominal pain Without abdominal pain
100%
90%
80% 86
70%
60% 66
Patients

50% 58
54
48 50
40%
40
30% 36 36
20%
10% 13
0%
<5 5 to <10 10 to 15-18 <400 400-600 >600 <300 300-320 >320
<15
Bicarbonate Glucose Serum Osmolality

*P<0.05. †P<0.01. ‡P<0.0001.

Umpierrez G, Freire AX. J Crit Care. 2002;17:63-67.
TREATMENT
RECOMMENDATIONS
28
 Management of DKA and HHS

• Replacement of fluids losses

• Correction of hyperglycemia/metabolic acidosis
• Replacement of electrolytes losses
• Detection and treatment of precipitating causes
• Conversion to a maintenance diabetes regimen
(prevention of recurrence)

Kitabchi AE, et al. Diabetes Care. 2009;32:1335-1343

Alspach, 2005.
 Management of DKA in adult
(Canadian Diabetes Association, 2013)

30
 Suggested Initial Rate of Fluid
Replacement*
Hours Volume
1st hour 1000 – 2,000 mL
2nd hour 1000 mL
3rd-5th hours 500 – 1000 mL/hour
6th-12th hours 250 – 500 mL/hour

*Average replacement after initial hemodynamic resuscitation with normal saline when
indicated

Chaithongdi N et al. Hormones (Athens). 2011;10:250-260.

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FINDING THE CAUSE AND
PREVENTING RECURRENCE
32
Possible Precipitating Causes or Factors
in DKA: Type 1 Diabetes
• Nonadherence to insulin regimen or psychiatric
issues
• Insulin error or insulin pump malfunction
• Poor “sick-day” management
• Infection (intra-abdominal, pyelonephritis, flu)
• Myocardial infarction
• Pancreatitis
• Other endocrinopathy (rare)
• Steroid therapy, other drugs or substances
33
Possible Precipitating Causes or Factors
in DKA: Type 2 Diabetes
• Nonadherence to medication regimen
• Poor “sick-day’ management
• Dehydration
• Renal insufficiency
• Infection (intra-abdominal, pyelonephritis, flu)
• Myocardial infarction, stroke
• Other endocrinopathy (rare)
• Steroid therapy, other drugs or substances

34
Predischarge Checklist

• Diet information
• Glucose monitor and strips
(and associated prescription)
• Medications, insulin, needles
(and associated prescription)
• Treatment goals
• Contact phone numbers
• “Medic-Alert” bracelet
• “Survival Skills” training

35
 Education in Type 1 Diabetes
to Prevent DKA
• Recognize symptoms and findings that require
contact with a healthcare provider
• Prevent ketoacidosis through self-management
skills:
– Glucose testing
– Appropriate use of urine acetone testing
– Appropriate maintenance of insulin on sick days
– Use of supplemental insulin during illness
• Address social factors

36
 Summary

• DKA and HHS are life-threatening emergencies

• Management involves
– Attention to precipitating cause
– Fluid and electrolyte management
– Insulin therapy
– Patient monitoring
– Prevention of metabolic complications during recovery
– Transition to long-term therapy
• Patient education and discharge planning should
aim at prevention of recurrence

37
 ASUHAN KEPERAWATAN
PASIEN DENGAN
HIPEROSMOLAR NON KETOTIK
 KASUS

• Seorang laki-laki berusia 60 tahun, ± 6 jam SMRS

klien dibawa ke RS Al-ikhsan dengan keluhan
sering merasa haus, sering buang air kecil dan
sering merasa lapar. Klien didiagnosa DM,
kemudian klien diperbolehkan pulang, pada saat
dirumah klien mengalami penurunan kesadaran
sehingga klien dibawa kembali ke RS Al-Islam.
GDS klien 500 mg/dl sehingga klien dirujuk ke
RSHS.
• Terdapat riwayat mual, namun klien tidak memiliki
riwayat muntah. Hasil pengkajian didapatkan
Pasien mengalami penurunan kesadaran dengan
GSC 9 E2M5V2, akral dingin, kulit pucat dan
kering, CRT > 3 detik, SpO2 88,4%. Klien juga
terlihat sesak nafas. Tanda-tanda vital: Nadi: 98
x/menit, RR: 28 x/menit, TD : 100/70 mmHg, Suhu :
36,4oC.
 HASIL LABORATORIUM

• F:\HONK\Pemeriksaan [Link]
 pengkajian
Primary Survay

Airway Breathing Circulation

• Tidak terdapat secret • Klien tampak sesak • Akral dingin
• Tidak terdapat benda asing • RR : 28 x/menit • Warna kulit pucat
• Tidak terdapat sisa makanan • Terdapat penggunaan
• Tidak terdapat sisa otot bantu nafas
• Tekstur kulit kering
muntahan • Pergerakan dinding dada • TD : 100/70 mmHg
• Tidak terdapat sumbatan simetris • N : 98 x/m
pada hidung dan mulut
• Tidak terdapat tanda fraktur
• Terdapat PCH • S : 36,4o C
cervical • Suara paru resonan • CRT > 3 detik
disemua lapang paru
Disability Eksposure
• GCS 9 (E2M5V2) • Tidak terdapat luka dibagian
• Pupil simetris tubuh
• Pupil mengecil ketika
dirangsang dengan cahaya
• Pasien mengalami
penurunan kesadaran
Secondary Survey

History
Sign / Symptomp :
Keluhan utama: Klien menglami
Pasien datang dengan penurunan kesadaran penurunan kesadaran
sejak 2 hari yang lalu

Alergi : Post medication history :

Medication :
Keluarga klien mengatakan ± 6 bulan yang lalu, klien
Keluarga klien mengatakan
bahwa klien tidak memiliki dirawat di RS dengan
bahwa klien mengkonsumsi
riwayat alergi terhadap keluhan klien sering merasa
obat-obatan untuk
makanan, obat-obatan haus, sering buang air kecil
mengatasi mual,
maupun cuaca. serta sering merasa lapar.
 Last eat / drink : • event:
Klien tidak makan dan minum • Menurut keluarga pasien
sejak ± 2 hari yang lalu karena setelah pulang RS al ihsan
mengalami penurunan
klien mengalami penurunan kesadaran  ke al islam GDS
kesadaran. 500  RSHS.
2. Tanda-tanda vital
• Nadi : 98 x/menit
• RR : 28 x/menit
• TD : 100/70 mmHg
• Suhu : 36,4o C
• SpO2 : 88,4 %
• GCC : 9  E2 M5 V2  kesadaran : Sopor

3. Pengkajian Head To Toe

 Terapi

1. Infus 2A :
• 1000 cc/ ½ jam
• 1000 cc / 1jam
• 1000 cc / 2 jam
• 1000 cc/4 jam
2. Insulin Bolus 0,5 UI dilanjutkan 5 UI / jam
3. Koreksi Hipokalemi dengan KCL 7,46 % 25 Meq
dalam RL 500 CC/ 6 Jam
 Analisa keperawatan

• F:\HONK\Analisa [Link]
 Diagnosa keperawatan

1. Kekurangan volume cairan berhubungan dengan

hiperglikemi
2. Ketidakseimbangan elektrolit berhubungan dengan
gangguan mekanisme regulasi
3. Resiko gangguan perfusi jaringan serebral
 Intervensi keperawatan

• F:\HONK\Intervensi [Link]