Diabetic Ketoacidosis

Albano, Bautista, Cimatu,

Purificacion, Sieterales

General Data

A.R.
11 years old
Male
Roman Catholic
born on March 16, 2005
Dasmarias City
admitted for the 2nd time at DLSHSI UMC
March 2, 2016 at around 10:00PM

Chief Complaint
Generalized body weakness

History of Present Illness

One day PTC
(+) generalized body weakness
(+) 1 episode of non projectile, nonbillous vomiting of previously
consumed food
(+) non-rotatory dizziness
(-) fever, (-) diarrhea, (-) decrease in
sensorium
(-) consult , (-) medications

History of Present Illness

12 hours PTC
(+) Persistence of generalized body
weakness
(+) 1 episode of non projectile, non-billous
vomiting of previously consumed food
(+) non-rotatory dizziness
(+) vague generalized abdominal pain,
constricting in
character

History of Present Illness

12 hours PTC(-) DOB/ shallow breathing, (-) decrease in
sensorium
CBG taken via homekit which revealed a
CBG of 311 mg/dL with ketones detected thus
prompting consult

Review of Systems

General
(-) poor activity (-) weight loss

Integument
(-) wound (-) pallor (-) hyperpigmentation
(-) hypopigmentation (-) erythema (-) nail
clubbing

Head and Neck

(-) stiffness (-) mass (-) distension of veins (-)

swelling

Eyes

(-) redness (-) discharge

Ears

(-) discharge

 Nose and Sinuses

(-) watery discharge (-) nasal flaring (-) epistaxis
(-) obstruction

Mouth and Throat

(-) dry throat (-) ulcers

Respiratory
(-) dyspnea (-) hemoptysis (-) tachypnea

Cardiovascular
(-) dyspnea

(-) palpitation

 GIT
(-) vomiting (-) diarrhea (-) abdominal distention
(-) constipation (-) hematemesis (-)
hematochezia

GUT
(-) frequency (-) polyuria (-) oliguria (-) palpable
mass

Hematologic
(-) easy bruising (-) easy bleeding (-) pallor
(-) received blood transfusion

 Endocrine
(-) polyuria (-) polydipsia (-) diaphoresis

MSS/Extremities
(-) fractures (-) joint pains

Nervous System
(-) seizures (-) syncope (-) tremors

Autonomic Deficiency
(-) fecal incontinence (-) urinary incontinence

Past Medical History

Diagnosed with DM Type I in 2014
Previously admitted in 2014 for DM Type I
Current medication:
Human Regular Insulin + Isophane Human
Inaulin 20 units AM, 14 units PM

Past Medical History

No history of allergy, asthma, primary
complex, infectious diseases congenital
heart disease, congenital, pulmonary
disease, kidney and liver diseases.
No surgical operation, injury, accident
were elicited.

Family History
(+) DM Type II- Maternal side
(+) Hypertension- Maternal side
(+) Colon Ca- Maternal side
No family history of asthma,
tuberculosis, liver disease, lung
disease, kidney disease, epilepsy,
and congenital anomalies.

Birth & Maternal History

Patient was born term to a 26-year old
G1P1 (1001) via VSD in a hospital
attended by an OB
No history of GDM, Maternal infection/
hyper or hypothyroidism, Gestational
Hypertension

Birth & Maternal History

No medications taken during pregnancy
No complications during pregnancy, both
intrapartum and postpartum were noted.

Developmental History
Patients development is at par with age
Specific timing of developmental
milestones cannot be recalled by
grandmother

Nutritional History
The patient was exclusively breastfed
Milk formula, ratio, amount and frequency
cannot be recalled by grandmother
Solid food: 7 months
Table food: 15 months

Immunization History
Vaccine

Given

BCG1

Yes

DPT
1st dose
2nd dose
3rd dose

Yes
Yes
Yes

OPV

Yes

Hepa B
1st dose
2nd dose
3rd dose

Yes
Yes
Yes

MMR
1st dose

No

Personal & Social History

Father is an OFW, a non-smoker, a nonalcoholic beverage drinker
Mother is an OFW, a non-smoker, a nonalcoholic beverage drinker
Under the care of her grandmother and
aunt
Currently in first year high school
Diet: currently on diabetic diet

Gynecologic History
Menarche: 11 years old (February
2016)
Interval: Presently irregular

PHYSICAL EXAMINATION

Physical Examination
General Survey
The patient is well developed, well
nourished, conscious, not in cardiorespiratory distress and looks his
chronological age. IV line is inserted
on his left dorsal hand.

Vital Signs
BP: 90/60 mmHg, right arm, lying
position
HR: 121 bpm
RR: 24 cpm
Temperature: 36.5 degrees Celsius
Weight: 33 kg

Regional Examination
Integumentary
The skin is moist, smooth, and fair. There
was no pallor, jaundice, or any
discoloration. Patient is afebrile and not
cold to touch. There is prompt return of
skin after finger pressure is applied. No
excessive moisture nor sclerosis was
noted. No peripheral cyanosis was noted.
Maculopapular rashes were noted in the
trunk and extremities. Polumorphous
exanthem in the groin area.

 Head and Neck

Hair color is black with fine
texture. Head is normocephalic,
symmetrical with no mass or
lesion. Facial features are
symmetrical. No cervical
lymphadenopathy noted.
Eyes
Eyes are symmetrical and
responsive to light. Full EOM were
also assessed. Slightly sunken
eyeballs

 Nose
Nose is symmetrical with no masses
and lesions. Nasal septum is
midline.

Ears
No obvious mass or lesion was
noted at the external ear.

Oral Cavity and Pharynx

Uvula was midline. There were no
lesions or masses. Lips were dry.

Chest and Lung

Inspection

Chest is symmetrical, no
deformity, mass or retraction
noted.
Palpation

Symmetrical chest expansion

Percussion

Not done
Auscultation

Patient has clear breath sounds.

No adventitious breath sounds
noted.

Cardiovascular
Inspection
No bulging was noted

Palpation
No heaves or thrills.

Auscultation
The patient has regular rhythm.
Apex beat at 5th ICS LMCL. No
murmur was appreciated.

Abdomen
Inspection

Abdomen is globular, no scar, lesion,

discoloration, mass or visible
peristalsis was noted.

Auscultation
12 bowel sounds per minute was
noted. No bruit.

Percussion
Not done

Palpation
No tenderness and organomegaly were
elicited.

EXTREMITIES
There were no masses, lesions, gross
deformities
Full and Equal peripheral pulses
There were no tenderness, crepitus or
limitation in ROM

Neurologic Examination
Mental Status Examination
COMPONENT

REMARKS

Level of Consciousness

Cooperative towards the

examiner
Awake

Cognitive Function

Able to demonstrate social

behavior
Goodnonverbal language
Active and playful

Grapho-motor/visuomotor
skills

Able to lookand able to eat

on his own

Neurologic Examination
CN
I
II

FINDINGS
not done
(+) Directand Consensuallight reflex
Visual acuity:not done
Visual fields: able to respond or turn toa non-audible
stimulifrom the side
Fundoscopy:not done
Ciliospinalreflex:not done

III, IV, VI

Midpositionof eyes at rest

Pupillaryequally reactive to light andaccomodation
Good chewing movement
Good jaw movements; no deviation
Frequency of blinking not increased or decreased
Facial sensation is intact

Neurologic Examination
VII
VIII

IX, X

XI

XII

(-) facial asymmetry

(-) facial paralysis
(+) gross hearing
Able to look with just eyes and
not with head
(+) swallowing(+) cough
Normal uvulaposition; (+)
palatal elevation
(+) Gag Reflex
Head can move side-to-side
(+) shoulder shrug
(-) atrophy
(-) lateral deviation of tongue
(-)fasciculations

Neurologic Examination
Motor
System

b. Palpation
o Normal muscle bulk
o Body is symmetrical

a. Inspection
o General activity: active
o (-) tremor
o (-) involuntary movement

o (-) jointmalalignment
o (-)fasciculations
o Normal muscle tone, (-) spastic,
(-)flaccid

 Meningeals

(-) kernigs and brudzinkis

Reflexes
Primitive/ Pathologic Reflexes
(-) Palmar Grasp on hand
(-) Babinski

Discussion

DIABETES MELLITUS
common, chronic, metabolic syndrome
characterized by hyperglycemia (cardinal
biochemical feature)
Type 1 DM( T1DM) deficiency of insulin
secretion due to pancreatic -cell damage
Type 2 DM( T2DM) consequence of insulin
resistance occurring at the level of skeletal
muscle, liver, and adipose tissue, with various
degrees of -cell impairment

TYPE 1 Diabetes Mellitus

Insulin-dependent diabetes mellitus
(IDDM) or juvenile diabetes
Characterized by low or absent levels
of endogenously produced insulin
dependence on exogenous insulin to
prevent complications

Most commonly diagnosed at a

median age of 7 to 15 yr

TYPE 1 Diabetes Mellitus

Destruction of pancreatic islet cells
Autoimmune
drugs or chemicals, viruses,
mitochondrial gene defects,
pancreatectomy, and ionizing radiation

PATHOPHYSIOLOGY of T1DM
INSULIN
permit controlled disposition of ingested
food as energy for immediate or future use
Released by the pancreatic islet cells

regular swings between

Postprandial= high-insulin anabolic state
the fasted= low-insulin catabolic state that
affect liver, muscle, and adipose tissue

PATHOPHYSIOLOGY of T1DM
FOOD INTAKE with low insulin Hyperglycemia
Producing an osmotic diuresis (glycosuria)

loss of calories and electrolytes, as well as

the persistent dehydration PHYSIOLOGIC
STRESS STRESS HORMONES
epinephrine, cortisol, growth hormone, and glucagon
metabolic decompensation by further impairing
insulin secretion & antagonizing its action
promoting glycogenolysis, gluconeogenesis, lipolysis,
and ketogenesis
decreasing glucose utilization and glucose clearance

Diabetic Ketoacidosis
leading cause of morbidity and
mortality in children with type 1
diabetes mellitus (T1DM),
case fatality rate 0.15 % to 0.31 %

occur in children with type 2 DM

(T2DM)
African-American descent

Diagnosis :
International Society for Pediatric and
Adolescent Diabetes (ISPAD) in 2014 biochemical criteria
Hyperglycemia, defined as a blood glucose
of >200 mg/dL (11 mmol/L) AND
Metabolic acidosis, defined as a venous pH
<7.3 or a plasma bicarbonate <15 mEq/L
(15 mmol/L) AND
Ketosis, ideally determined by serum betahydroxybutyrate as measured in the
laboratory or by a point-of-care testing
device.

Risk Factors: newly diagnosed type

1 diabetes
Young age (<5 years of age and
especially <2 years)
Low socioeconomic status
Delayed diagnosis
Children living in countries with low
prevalence of type 1 diabetes

Risk Factors: established type 1

diabetes mellitus
Children with poor metabolic control
Gastroenteritis with vomiting and dehydration
Peripubertal and pubertal adolescent girls
history of psychiatric disorders (including
eating disorders), or unstable family
circumstances
limited access to medical circumstances
Inadvertent or intentional omission of insulin,
including failure of an insulin pump

Signs and Symptoms:

Polyuria
Polydypsia
Tachycardia
Fatigue
Decreased energy and activity
Irritability
Physical signs of dehydration

Signs and Symptoms

Polyphagia
Anorexia
Nausea
Vomiting
Abdominal pain
Hypervetilation
Kussmauls breathing
Hyperpnea
Tachypnea
Fruity Breath

Signs and Symptoms

Drowsiness
Lethargy
Obtundation

Complications

Cerebral Edema
Cognitive Impairment
Venous thrombosis
Aspiration
Cardiac Arrhythmia

Prevention
Early detection of risk factors
Glycemic control

EMERGENCY ROOM

S
Known type 1 diabetic for 2 years
maintained on Regular Insulin
20u ODAM; 16u ODPM
2 days history of dizziness, body
weakness with decreasing
appetite
Presenting with vomiting x 2
episodes with no abdominal pain
CBG at home 311 with ketones
#1 Hyperglycemia

O
PE: Stable VS: 110/80, 84, 20,
35.9
Awake, alert and conscious
No cyanosis/ pallor, good skin
turgor, slightly sunken eyeballs
Dry lips, moist oral mucosa
CBS
Normal rhythm, regular rate (-)
murmur
SNABS
Good pulses, good capillary refill
time
No neurologic deficits

EMERGENCY ROOM
A
Type 1 Diabetes Mellitus, uncontrolled
T/C Diabetic Ketoacidosis

For CBG
For Urinalysis with ketones
For ABG, 15L ECG
Hook to cardiac monitor

EMERGENCY ROOM

CBG: 365mg/dL
Urinalysis with Ketones
Glucosuria +2
Ketonuria +3
ABG:
Metabolic acidosis,
partially compensated
15L ECG: normal for age

IVF started
TX:
REGULAR INSULIN 5U SQ
now
Advised ADMISSION

Admitting Diagnosis
DIABETIC KETOACIDOSIS, MILD
TYPE 1 DIABETES MELLITUS,
UNCONTROLLED

Goals of therapy

To correct dehydration
To correct acidosis
To reverse ketosis
To restore blood glucose to near
normal
Identify precipitating event

Emergency Assessment

Measure blood glucose

Weigh patient
Assess severity of dehydration
Assess level of consciousness
Obtain blood sample for lab
measurements
Perform Urinalysis with ketones
ECG

Additional Measures

Secure Airway
Give oxygen
Hook to cardiac monitor
IV access
Give antibiotics
Catheterization, if needed

Need for ICU?

Long duration of symptoms

Compromised circulation
Depressed level of consciousness
Increased risk of cerebral edema
<5 years old
Low pCO2
High BUN

COURSE IN THE WARDS

S
(+) pain over extraction site
(-) abdominal pain
(-) vomiting
(-) weakness
(-) DOB
(-) tremors
(-) polyuria
(-) changes in sensorium
#1 Hyperglycemia

O
PE: Stable VS: 100/70, 86, 19,
36.1
Awake, alert and conscious
No cyanosis/ pallor, slightly
sunken eyeballs
Dry lips, moist oral mucosa
CBS
Normal rhythm, regular rate (-)
murmur
SNABS
Good pulses
No neurologic deficits
CBG: 114-340mg/dL

COURSE IN THE WARDS

A
Diabetic Ketoacidosis - Mild
Type 1 Diabetes Mellitus

P
IVF PNSS IL x 106-107cc/hr, if CBG > 200
IVF D5 0.45 NaCL 1L x 106-107cc/hr, if CBG <200
Regular Insulin 5u SQ q3, if CBG <180 adjust to 4u
For CBCPC
For HbA1C
For blood ketones q6
Monitor VS q1 and NVS

Fluid Replacement
Rationale:
Restore circulating volume
Replaced sodium and fluid deficit
Improved glomerular filtration with
enhanced clearance of glucose and
ketones

Fluid Replacement
Resuscitation fluids
0.9% saline; 10-20mL/kg over 1-2 hours
If in shock, isotonic saline; 20mL/kg
bolus

Deficit replacement fluids

Replacement + FM for at least 4-6h

Insulin therapy
Rationale
Restore normal cellular metabolism
Normalize blood glucose concentration
Suppress lipolysis and ketogenesis

Insulin therapy
IV Insulin infusion 1-2h after fluid
replacement
Dose: 0.05-0.1u/kg/h
May decreased accordingly, to prevent
hypoglycemia
If given for prolonged period of time,
may induce hypokalemia

Gradual correction reducing blood

glucose by 50-100mg/dL/hr

Insulin therapy
If continuous IV administration is not
possible and for uncomplicated DKA
Hourly/2-hour SC or IM administration of
short or rapid acting insulin
Initial dose: 0.3u/kg SC then reduce to
0.1u/kg every hour or 0.15u-0.2 every 2
hours (Insulin lispro or aspart)

Insulin Preparation

Electrolyte correction
Potassium replacement
Start after initial volume expansion and
concurrent with starting insulin therapy
Initial: 0.5mmol/kg/h (max)
Subsequent potassium replacement
therapy based on serum potassium level

COURSE IN THE WARDS

S
(-) pain over extraction site
(-) abdominal pain
(-) vomiting
(-) weakness
(-) DOB
(-) tremors
(-) polyuria
(-) changes in sensorium
Able to tolerate diet

O
PE: Stable VS: 100/70, 86, 19,
36.1
Awake, alert and conscious
No cyanosis/ pallor, nonsunken
eyeballs
Slightly dry lips, moist oral
mucosa
CBS
Normal rhythm, regular rate (-)
murmur
SNABS
Good pulses, good capillary refill
No neurologic deficits, GCS 15
CBG: 80-274mg/dL

COURSE IN THE WARDS

O
CBG: 80-274mg/dL
Blood Ketones: 0.0 0.5 mmol/L
HbA1C: 13.6%
CBCPC: within normal limits

COURSE IN THE WARDS

A
Diabetic Ketoacidosis Mild, Resolved
Type 1 Diabetes Mellitus

IVF to consume
MGH
HM: Scillin M30 24u ODAM, 16u ODPM

Resolution?
When oral fluid is tolerated, reduced
IVF accordingly
If planning to shift insulin to
subcutaneous injection, before
mealtime and 15-30min (rapidacting insulin) or 1-2h (regular
insulin) before stopping insulin
infusion

Algorithm

Algorithm

Patient Education
Nutritional management
Continuous glucose monitoring

Healthy Plate

Timing of MBG
At bedtime, during the night,
overnight fast
During the day prior meals, after
food intake (2hours after meal)
In association with vigorous exercises
During intercurrent Illness

 THANK YOU!!!!