4. There is ACUTE LIFE THREATENING PROBLEM.
So we will activate emergency response system
as appropriate for setting
Rush to resus. room
Call for help - doctors
Attach high flow oxygen.
Attach cardiac monitor and ECG electrodes
5.
6. EVALUATE:
PRIMARY ASSESSMENT:
Airway: Clear
Breathing: Respiratory rate of 48/min , no added sounds ,
spo2 95% off O2, No indrawing , NVB, b/l equal air entry
Circulation: heart rate 140/min, central and peripheral pulses
are WEAK , CRT more than 3 sec, BP 100/60mmhg
Disability: responds to verbal, RBS: 47 mg/dl, pupils = BERL
Exposure: temperature 37.6C , no rashes, dry mucous
membrane, poor skin turgor, sunken eyes
7. After primary assessment we categorize the pt’s state as
compensated shock most likely HYPOVOLEMIC Shock and
intervention was done accordingly:
Maintain IV/IO line
Analyze cardiac rhythm ( sinus tachycardia)
20ml/kg 0.9% Normal saline first bolus was given (push
and pull technique)
4ml/kg 10% Dextrose bolus was given
Pt. was catheterized.
After each bolus, chest was ascultated for crepts, liver for
enlargement and HR for improvement.
3 boluses of N/S was given and pt. improved.
8. SECONDARY ASSESSMENT:
SAMPLE History:
Signs and Symptoms: Loose motion for 3 days, 7
episodes/day, watery in consistency, large in quantity, foul
smelling. Vomiting for 3 day, 3 episodes/ day, large in
quantity, non-projectile, white in color, containing food
particles, asso. With food and water intake. Pt. became
lethargic for which he was taken to ER
Allergies: none
Medication: none
9. Past medical history : INSIGNIFICANT
Last meal: a biscuit and few sips of juices 4
hours ago
Events: His appetite decreased and Pt. became
lethargic for which he was taken to ER.
11. HEAD TO TOE EXAMINATION:
HEENT:
Unremarkable
RESPIRATORY EXAMINATION :
Normal vesicular breathing .
No basal crepts.
CARDIOVASCULAR:
S1+S2+O
Tachycardia.
Apex beat palpable at 4th ICS medial to mid clavicular
line.
12. ABDOMINAL EXAMINATION:
Soft , non distended
No visceromegaly
Gut sounds audible
Severe dehydration present.
PELVIS / EXTREMITIES:
Unremarkable
BACK :
Unremarkable
CENTRAL NERVOUS SYSTEM :
GCS = 15/15
Conscious and Alert now .
14. INTERVENTION:
Deficit – bolus = 1600 - 960 = 640
DEFICIT FLUID: 640ml 0.9% Dextrose saline was given.
320ml over 8 hrs. and rest 320 ml over next 16 hrs.
MAINTENANCE FLUID: 1300 ml 0.9% Dextrose saline
given. 440 ml over 1st 8 hrs and the rest 860 ml in the
next 16 hrs.
Ongoing losses were replaced by 100 ml of 0.9% N/S
Inj. Ceftriaxone 1.2 g IV X OD.
15. LABS INVESTIGATIONS :-
Hb 10.3 10.3
Hct 35 30.8
Tlc 16.3 11
N 85.3 56
L 8 23
Plt 596 565
BUN 29 15
Cre 1.4 0.5
Na 137 135
K 2.9 3.9
Cl 104 100
Ca 9.1 9
Mg 2.5 2.4
Pho 5.2 5.3
16. LABS INVESTIGATIONS
STOOL D/R:
pH = acidic
Consistency = loose
Colour = yellowish
Red cells = nil/ HPF
Pus cells = 10-12/HPF
STOOL C/S: No bacterial growth
17. PROGRESS DURING HOSPITAL
STAY:
Urine output was 2 ml/kg/hr.
Potassium was low. So, KCl was added in maintenance
fluid. 2 mEq KCl in every 100 ml of fluid
By day 2, child was stabilized and orally allowed.
Replacement fluid were given orally in the form of ORS.
UCE were repeated which normalized.
Frequency of stool reduced
Child was discharged after 7 days of IV antibiotic.
20. Shock:
Shock is characterized by body’s inability to deliver
adequate oxygen to meet the metabolic demands of vital
organs and tissues.
Pathophysiology:
After an initial insult triggering shock leading to
inadequate oxygen delivery to organs and tissues,
compensatory mechanisms attempt to maintain BP by
increasing cardiac output, HR and systemic vascular
resistance (SVR) through sympathetic nervous system
activation and neurohormonal response.
21. And to optimize O2 delivery to the tissues, body also
increases O2 extraction and redistributing blood flow
to the brain, heart and kidneys at the expense of skin
and GI tract.
Respiratory compensation includes greater CO2
elimination in response to metabolic acidosis which
resulted due to deficiency in O2 delivery and a shift to
anaerobic metabolism.
These responses lead to an initial
state of COMPENSATED SHOCK but if treatment is not
initiated or inadequate during this period,
DECOMPENSATED SHOCK develops with hypotension
and tissue damage that may lead to MULTIPLE ORGAN
DYSFUNCTION and ultimately to DEATH.
22. TYPES OF SHOCK:
HYPOVOLEMIC SHOCK:
Most common cause of shock, caused by decreased
circulatory volume.
E.g. haemorrhage or fluid loss ( diarrhoea or
CARDIOGENIC SHOCK:
Caused due to impaired heart function.
E.g. Acute coronary syndrome, valve failure,
or acquired myopathies etc.
23. OBSTRUCTIVE SHOCK:
Due to any lesion that creates a mechanical barrier
that impedes cardiac output.
E.g. cardiac tamponade, tension pneumothorax,
pulmonary embolism, etc
DISTRIBUTIVE SHOCK:
Caused by pathologic peripheral vasodilation.
E.g. sepsis, anaphylaxis, neurogenic
28. DEFICIT:
Estimation of deficit: by assessing dehydration.
Mild dehydration = 5-7%
Moderate dehydration = 7-10%
Severe dehydration = 10-15%
Fluid: Isotonic fluids( Ringer lactate or 0.9% DS)
Amount: For every 1% dehydration, 10ml/kg fluid
given.
Technique: Half of the total fluid was given in 1st 8
and the remaining half in the next 16 hrs.