CASE 1

A 10 years old boy was admitted, with history of profuse diarrhea 10X/day for
the last 3 days. He was otherwise well before this. He’s been a regular
customer of an ice kacang stall situated near his school. Since the morning of

DEHYDRATION
admission, he’s not been able to hold down any food /water given to him

Clinically, his eyes were sunken, and skin turgor was laxed.

& SHOCK
PR 120/minute, small pulse volume.
Though conscious, he was very drowsy.
His blood pressure was 90/60 mmHg.
BUN 14 mmol/L, K⁺ 2.5mmol/L, Na⁺ 135 mmol/L
ME121 GROUP C1 & C2

Discuss the immediate management of the patients in

Key points from the case: detail.
Our patient : Severe dehydration -> treat quickly -> Plan C
● Profuse diarrhea x10/day for 3 days + Hx of eating ice kajang ->
Possible Acute gastroenteritis
● Severe dehydration -> signs :
○ Sunken eyes
○ Skin turgor laxity
● Hypovolemic shock -> signs:
○ Hypotension
○ Tachycardia
○ Drowsiness
● Investigations :
○ BUN : 14 mmol/L - High ( normal : 2.5 - 6.0 mmol/L) -> indicates AKI
due to hypovolemia ?
○ K⁺ 2.5mmol/L - Hypokalemia ( Normal: 3.5- 5.0 mmol/L)
○ Na⁺ 135 mmol/L - Borderline ( Normal : 135- 145 mmol/L)

Plan C:

1. Assess - ABCs
a. Airway
b. Breathing
c. Circulation

2. Start IV (Intravenous) or IO (Intraosseous) fluid immediately

a. If patient can drink -> ORS by mouth while drip being set up
b. Initial fluids for resuscitation of shock : 20 ml/kg of 0.9% Normal Saline or
Hartmann’s solution - rapid IV bolus (refer to the table in the next slide)
c. Repeat if necessary -> until patient out of shock
d. Review patient after each bolus
e. If not responsive to fluid bolus -> consider other causes of shock e.g
septicemia
f. Once circulation restored -> commence rehydration + maintenance +
replace ongoing losses

Note :
Reassessing hydration status every 1-2 hours and infusion adjustment - very
important
 ● Severe dehydration should be treated with intravenous fluids until the patient is
stabilized (i.e., circulating blood volume is restored).
● Treatment should include 20 mL per kg of isotonic crystalloid (normal saline or
lactated Ringer solution) over 10 to 15 minutes.
● monitoring of the patient's pulse strength, capillary refill time, mental status, and
urine output.
● Stabilization often requires up to 60 mL per kg of fluid within an hour.
● After resuscitation is completed and normal electrolyte levels are achieved, the
patient should receive 100 mL per kg of ORT solution over four hours, then
maintenance fluid and replacement of ongoing losses.

Deficit Electrolyte Disturbance : Correct hypokalemia

● Calculated following the estimate of the ● Treat the underlying diarrhoea

degree of dehydration expressed in % of
● Oral supplementation: Oral Potassium Chloride (KCL), to a
bodyweight.
● Use an isotonic solution for replacement of
maximum of 2 mmol/kg/day in divided doses
the deficit, e.g. 0.9% saline.
● Reassess clinical status and weight at 4-6 ● Intravenous correction: through IV infusion , NEVER bolus
hours, and if satisfactory continue. injection
● If child is losing weight, increase the fluid ○ Maximum concentration via a peripheral vein is 40
and if weight gain is excessive, decrease mmol/l.
the fluid rate. ○ Maximum infusion rate is 0.2mmol/kg/hour (in
● Replacement may be rapid in most cases of non-intensive care setting.)
gastroenteritis (best achieved by oral or
nasogastric fluids)
● Ongoing losses - These are best measured
and replaced. Any fluid losses > 0.5ml/kg/hr
needs to be replaced.
●

What other investigations would you do?

Other measures required to be taken before he’s
1. FBC ● ↑ Hb and Hct -> Hemoconcentration due allowed to be discharged.
Hypovolemia

1. Once the child is able to feed -> continue normal feeding

2. Renal Profile ● BUN - done
● May show signs of AKI ● Creatinine 2. Drugs e.g Antibiotics, antiemetics, antidiarrheal - not
● ↑ BUN/creatinine ratio (> 20:1), typically
secondary to renal hypoperfusion recommended

3. ABG ● Metabolic acidosis with ↓ HCO3- (due to severe 3. Education on food hygiene
diarrhea)

4. Urine ● ↑ Specific gravity and ↑ osmolarity -> indicates

urine concentration

5. STOOL: MICROSCOPY
● Culture & sensitivity - persistent diarrhoea
 CASE 2
A 9 month-old-infant was brought in by his mother with history of passing loose watery stool Important points from the history Interpretation of the history
> 5X/day X 2/7. He is being taken care of by a babysitter, and on formula milk. On further
questioning the baby sitter said that she mixed 8 full scoop of milk with 5 oz of water. He is ● 9 month old infant ● Acute diarrhea -> risk of
also given nestum. ● Loose watery stool > 5x /day for 2 dehydration and electrolyte
His weight is 11 kg. paO2 75mmHg,
days imbalance
Temperature 38 °C. pco2 28mmHg,
BUN 12 mmol/l, ● On formula milk
PR 135 bpm, RR 45/ min,
ABG pH 7.2, Na⁺155 mmol/L, ○ 8 full scoop of milk with 5 oz ● Overfeeding-> osmotic
HCO3 15 mmol/L, K⁺ 6 mmol/L. of water + nestum diarrhea, gastrointestinal

In the ward, he was noted to be drowsy. And when the doctor started him on
discomfort, excess weight

intravenous therapy, he had a seizure.

gain and hypernatremia

Examination and investigation findings

● Weight : 11kg (>95th percentile in the ward, he was noted to be drowsy. And when the doctor started him
● Temperature : 38 degrees (febrile) on intravenous therapy, he had a seizure.
● Pulse rate : 135bpm
1. What are his problems
● RR : 45/min (raised)
● ABG ` ● Acute diarrhea -> risk of dehydration and metabolic acidosis
○ pH : 7.2 ● Overfeeding
○ HCO3 : 15mmol/L ○ Excessive weight gain
○ PaO2 : 75mmHg
○ Gastrointestinal upset
○ PCO2 : 28 mmHg
○ Hypernatremia
Interpretation : metabolic acidosis with
partial respiratory compensation ● Fever
● Developed a seizure after IV therapy
● BUN : 12mmol/L Diagnosis : Metabolic acidosis with
● Na+ : 155 mmol/L (hypernatremia) partial respiratory compensation
● K+ : 6 mmol/L ( hyperkalemia) secondary to dehydration

Management

● Manage the seizure

○ Rapid correction of fluid in a patient with hypernatremia can lead to cerebral
oedema and convulsions
○ ECF becomes more hypotonic than the ICF -> fluid shift into the cells
● Manage hypernatremic dehydration
● Identify the signs and degree of dehydration
● Identify signs of shock
○ If patient is in shock, give volume resuscitation with 0.9% NS as requires with
Maintenance fluid requirement in this
bolus
child
○ Based on classification of dehydration correct fluid deficit
○ Give maintenance fluid and and replace ongoing loses
First 10kg : 10x 100 = 1000mls
● Cardiac monitoring for hyperkalemia + manage hyperkalemia with nebulised salbutamol Subsequent 1 kg : 1 x 50 = 50mls
with IV bicarbonate Total : 1050 mls over 24 hrs with 0.9%
● Educate on proper amounts of feeding NS D5%

CASE 3
AO a 10 year old boy, a known case of leukemia, is presently undergoing induction chemotherapy. For the
past 2 days, he had been febrile, with a temperature of 39°C - 40 °C.
Clinically, there was no identifiable focus of infection, although he had been having running nose and
coughing. He was prescribed erythromycin 250 mg 8 hourly orally. His fever persisted and on the third
day of fever, mother pointed out a couple of painful skin nodules around the anal region. He was
tachycardic, PR 120 bpm, BP 100/70. Full blood counts showed the following: Hb 10g/dL, TW 1.2 x 109/L, ANC
400, Platelets 8 x 109/L. CXR showed patchy consolidation in the right lobe.
Blood culture was taken and parental antibiotics were given. His condition however deteriorated. More
nodules were observed, now involving the buttocks. The 2 earlier nodules have now blackened. In
addition, petechiaes appeared all over the limbs. On the 6th day of illness, he had hematemesis.
Appropriate measures were taken by the doctor in charge. Blood culture was reported to be negative, He
was still febrile, temperature remaining 40 °C. He was anuric for the last 6 hours.
Soon after, his vital signs destabilized, BP reading between 89-70mmHg systolic, with diastolic
becoming unrecordable. All efforts to resuscitate him failed.
List down his problems as the disease progressed. Explain the
pathophysiology.
1. Leukemia → Undergoing induction chemotherapy [Decreased production of
neutrophils due to suppression of bone marrow myeloid progenitor cells +
damage to host barriers (GI and sinuses) → increased susceptibility to
infection]
2. Development of upper respiratory infection (characterised by fever, runny
nose and cough)
3. Painful skin nodules around anal region (a secondary skin infection
manifestation to a chronic infection with gram-negative organisms, usually
in immunocompromised patients)
4. Patient was tachycardic, PR 120 bpm, BP 100/70. Hb 10g/dL, TW 1.2 x 109/L,
ANC 400, Platelets 8 x 109/L. (TW and ANC are low due to
chemotherapy-related neutropenia, tachycardia is a compensatory
mechanism due to increased permeability of BV caused by inflammatory
reactions, platelets are low as they are used up due to increased
expression of pro-coagulants)

List down his problems as the disease progressed. Explain the

pathophysiology. How would you manage and investigate this patient?

To identify source of infection

Further history taking
1. CXR showed patchy consolidation in the right lobe. (progression of URTI to ● Family history of unwell individuals, contact history
LRTI [Bronchopneumonia]) ● Drug history (incl. Prophylactic and
immunosuppressant drugs)
2. Generalised petechiae across whole body (Disseminated intravascular ● Check vaccination history
coagulation occurs due to exposure to increased expression of ● Check for previous microbiologically-confirmed
pro-coagulants leading to microvascular coagulation) diagnoses

3. Blackened nodules (due to tissue hypoperfusion) Further physical examination

● Note for any CVLs (remove if CRBSI is suspected)
4. Patient becomes anuric, his vital signs destabilized, BP reading between ● Examination of the mouth for mucositis or gingivitis
89-70mmHg systolic, with diastolic becoming unrecordable. (Septic shock: ● Examine the ears, nose and throat for signs of URTI,
leading to organ failure, prolonged period of shock causes body not to be otitis media and sinusitis
able to compensate any further, leading to drop in BP and death) ● Respi examination to hear for breath sounds
● Abdominal examination to check for anal fissure and
new hepatosplenomegaly

Further investigations
● Blood culture (before initiating broad spectrum antibiotics)
● FBC, renal and liver function tests
● Abdominal ultrasound after 72 hours of fever, to assess whether there is
fungal involvement of the kidney and/or liver
● Swabs of any inflamed or discharging skin or mucous membrane sites,
especially purulent discharge, should be sent for microscopy and culture.
● #Chest Xray

If patient went into sepsis

Monitor progression
 Normal Circulatory State Pathophysiology of Shock
Oxygen is usually carried from the lungs to the tissues by the RBCs within
the circulatory system. Shock is an acute process characterized by the body's inability to deliver adequate oxygen to meet
the metabolic demands of vital organs and tissues.
1. Heart function:
● Circulation is determined by the heart’s functionality, represented by
cardiac output (CO). ● Insufficient O2 at the tissue level is unable to support normal aerobic cellular metabolism → shift to
CO= SV × HR less efficient anaerobic metabolism (causing lactic acidosis)
2. Blood vessels: intravascular volume, and vascular tone, integrity, and ● Compensatory mechanisms: attempt to maintain BP, CO & SVR.
patency ● Body: attempts to optimize DO2 to tissues by increasing O2 extraction and redistributing blood flow to
3. Blood composition
4. Blood pressure: SP/DP, MAP the brain, heart, and kidneys at the expense of the skin and GI tract.
5. Oxygen and nutrient delivery ● This leads to an initial state of compensated shock (BP maintained) & if treatment is not initiated/
● Oxygen delivery (DO2) is dependent on two factors, Cardiac output
inadequate, decompensated shock (with hypotension and tissue damage→ multisystem organ
(CO) and arterial oxygen content (CaO2)
DO2=CO×CaO2 dysfunction → death )

6. Waste removal

Pathophysiology of Shock
1. Extracorporeal Fluid Loss
Hypovolemic shock due to direct blood loss through hemorrhage/ abnormal loss of body fluids
(diarrhea, vomiting, burns, diabetes mellitus or insipidus, nephrosis).

2. Lowering Plasma Oncotic Forces

Hypovolemic shock may result from hypoproteinemia (liver injury, or as a progressive complication of
increased capillary permeability).

3. Abnormal Vasodilation
Distributive shock (neurogenic, anaphylaxis, or septic shock) occurs when there is loss of vascular
tone—venous, arterial, or both (sympathetic blockade, local substances affecting permeability,
acidosis, drug effects, spinal cord transection).

4. Increased Vascular Permeability

Sepsis may change the capillary permeability in the absence of any change in capillary hydrostatic
pressure (endotoxins from sepsis, excess histamine release in anaphylaxis).

5. Cardiac Dysfunction
Peripheral hypoperfusion may result from any condition that affects the heart's ability to pump blood
efficiently (ischemia, acidosis, drugs, constrictive pericarditis, pancreatitis, sepsis).

Hypovolemic Shock CO = SV x HR Types of shock

DEFINITION POTENTIAL CAUSES PATHOPHYSIOLOGY CLINICAL FEATURES
● Shock is the inability to provide sufficient perfusion of the oxygenated blood and
HYPOVOLEMIC Decreased ● Blood loss Fluid loss → decreased preload ● Tachycardia
substrate to tissues to meet metabolic demands preload ● Plasma loss → hypotension → tissue ● ↑ SVR
secondary to ● Water/electrolyte loss ischemia ● Hypotension
Hypovolemic shock results from loss of fluid from the intravascular space secondary to internal or
external losses
inadequate intake or excessive losses.
CARDIOGENIC Cardiac pump ● Congenital heart disease Myocardial contractility is ● Tachycardia
failure secondary ● Cardiomyopathies affected → systolic/diastolic ● Signs of
Causes: to poor ○ Infectious or acquired, dysfunction hypoperfusion
myocardial dilated or restrictive ● Severe systemic
function ● Ischemia hypotension
HAEMORRHAGIC NON-HAEMORRHAGIC ● Arrhythmias ● Respiratory distress
due to pulmonary
➔ Postpartum hemorrhage ➔ GI loss
congestion (not all)
➔ Upper GI bleeding ➔ Increased insensible fluid loss
DISTRIBUTIVE Abnormalities of ● Sepsis Initially → ↓ SVR (Vasodilation) → ● Early: Warm shock
➔ Blunt/penetrating trauma ➔ Third space fluid loss
vasomotor tone ● Hypoxia maldistribution of blood flow ● Late: Cold shock
➔ Ruptured aneurysm or hematoma ➔ Renal fluid loss
from loss of ● Poisoning away from vital organs → ● Tachycardia
➔ Arteriovenous fistula venous and ● Anaphylaxis compensatory ↑cardiac output → ● Hypotension
arterial ● Spinal cord injury significant decrease in both ● Vasoconstriction
capacitance preload & afterload
 CO = SV x HR Types of shock
DEFINITION PATHOPHYSIOLOGY CLINICAL FEATURES

SEPTIC Encompasses multiple forms A type of distributive shock → caused by If a child with suspected or proven infection has any
of shock an excessive inflammatory response to 2 of these clinical signs:
1. Hypovolemic shock: from disseminated infection → leads to fluid I. Core temperature < 36°C or > 38.5°C
intravascular fluid losses extravasation from the vascular space II. Inappropriate tachycardia or tachypnoea
through capillary leak and loss of intravascular volume III. Altered mental state
2. Cardiogenic shock: IV. Reduced peripheral perfusion/prolonged
myocardial depressant Effect on cardiac output capillary refill
effects of sepsis 1. Early: compensatory ↑ HR and
3. Distributive shock : contractility → ↑ CO Septic children can present with:
decreased SVR (hyperdynamic state or “warm 1. Cold shock
shock”) 2. Warm shock
Potential causes: 2. Late: ↓ preload and direct
● Bacterial myocardial depression by
● Viral cytokines → ↓ CO (hypodynamic
● Fungal state or “cold shock”)
(immunocompromised
patients are at risk)

Classification of dehydration Elicit a proper history

Assess

Look at child’s general Well, alert Restless or irritable Lethargic or unconscious Additional information that we should elicit in history taking: 6. Any signs of dehydration (dry cry, sunken eye,
condition 1. Feeding history decrease urine output)
- Frequency and amount of formula milk fed
Look for sunken eyes No sunken eyes Sunken eyes Sunken eyes - Breastfeeding history (frequency and duration) 7. Immunisation history
2. Fluid intake
Offer the child fluid Drinks normally Drinks eagerly, thirsty Not able to drink or drinks poorly - Water intake - Rotavirus?
- Additional solid food 8. Travel history
Pinch skin of abdomen Skin goes back immediately Skin goes back slowly Skin goes back very slowly (>2 3. Output
9. Medical history
seconds) - Urine output (frequency of changing diapers, fully-soaked?)
- Stool consistency (any blood in stool ?) - Recent infection?
Classify Mild dehydration ≥ 2 above signs: ≥ 2 above signs:
< 5% Dehydrated Moderate dehydration Severe dehydration 4. History of vomiting
5-10% Dehydrated > 10% Dehydrated
5. Sick contact

-
Treat Plan A Plan B Plan C
Give fluid and food to treat diarrhea Give fluid and food for some Give fluid for severe dehydration.
at home dehydration Provide food as soon as child
tolerates

*% of body weight (in g) loss in fluid (Fluid deficit) Ex: A 10kg child with 5% dehydration has loss 5/100 x 10000g = 500mLs of fluid deficit.

Investigations
Recognise clinical features of the different type of
shocks Hypotension is a late sign in children due to their ability to increase heart rate (HR)
and systemic vascular resistance (SVR) to maintain cardiac output (CO). Hence,
microcirculatory markers like serum lactate, mixed venous saturation (ScVO2)
Hypovolemic shock Cardiogenic shock Septic Shock
provide better information regarding tissue perfusion as well as response to
treatment
· Clinical Features: · Clinical Features: · Clinical Features:

● Cold, clammy extremities, ● Cold, clammy extremities,
slow capillary refill poor capillary refill
● Nondistended jugular veins ● Elevated JVP and distended
● Decreased skin turgor, dry neck veins
mucous membranes ● Clinical features of heart
● Features of underlying failure
etiology: e.g., signs of GI ● Features of underlying
bleeding, diarrhea etiology: e.g., chest pain,
palpitations, syncope,
new/worsening murmur
● Early (warm): flushed, warm
skin, normal capillary refill
● Late (cold) : cold, pale skin
with delayed capillary refill
● Features of sepsis: e.g.,
fever
● Features of underlying
infection: e.g., signs of
typical pneumonia,
meningismus
I. Complete blood count:
- Low hemoglobin and low hematocrit → hemorrhage → hypovolemic shock
- Neutropenia or leukopenia → sepsis → septic shock
II. Basic Metabolic Panel: End organ dysfunction
- Renal function test: high blood urea nitrogen , and high creatinine
- Liver function test
III. EKG and Troponins
- Show evidence of cardiogenic etiology (eg: arrhythmias, acute coronary
syndrome, signs of cardiomyopathy) → cardiogenic shock
IV. Chest X Ray:
- Pneumonia suggests sepsis
- Pulmonary oedema, cardiomegaly, and pleural effusion suggest cardiogenic
Acute management of shock
etiology
- Pneumothorax suggests obstructive aetiology
Assess
V. Echocardiogram:
- Cardiac abnormalities
Categorize
Treatment (fluid replacement w
VI. Urine analysis/ cultures: Electrolyte balance)
- Signs of infection
- Urine specific gravity and the presence of ketones can assist in the evaluation Monitoring and Reassessment
of dehydration - Restoration of CRT
VII. Lactate:
- Normal BP
- Elevated blood lactate levels → poor tissue oxygen delivery → all forms of - Normal Pulses
shock - Warm extremities
VIII. Arterial blood gas:
- Normal urine
- Metabolic acidosis (Increased lactic acid production caused by anaerobic - Normal mental status
metabolism and a compensatory increase in tissue oxygen extraction.)
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