ALGORITHMS IN MEDICINE

Edition - 2018

Medical Division
Command Hospital Air Force, Bangalore
ALGORITHMS IN MEDICINE

Editor - in - chief
Air Cmde DS Chadha

Editors
Gp Capt Kishore Kumar
Surg Lt Cdr RN Hiremath

Published by
Command Hospital (Air Force)
Bangalore

Edition 2018
Disclaimer

The endeavour of editors and authors is provide the readers with latest
information as per standard publications at the time of compilation. However, the
field of medicine is vast and rapidly evolving and it is possible that there may be
variance in the information provided. Therefore the readers are requested to confirm
the same from current literature.

The publication of book is not a commercial enterprise and the same is meant only
for postgraduate education. The author's views and material are based on standard
guidelines, textbooks and internet resources.

All rights reservedThis book is protected by copyright. No part of it may be

reproduced in any manner or by any means without written permission from the
editors.

Editorial Contributions
Cardiology-Air Cmde DS Chadha,Gp Capt G Keshavamurthy ,Lt Col Ratheesh Kumar J ,
Endocrinology - Wg Cdr Kumar Abhisheka
Gastroenterology -Gp Capt VR Mujeeb ,Gp Capt AS Prasad
Neurology - Col RK Anadure VSM, Wg Cdr Jitesh Goel
Oncology - Gp Capt Kishore Kumar
Pulmonology - Wg Cdr Safia Ahmed
Rheumatology - Wg Cdr Harish Kumar
Haematology - Wg Cdr Harshit Khurana
Nephrology - Wg Cdr D Mahapatra, Wg Cdr VK Jha

Published by
Commanad Hospital (AF) Bangalore

Printed by:
AK Enterprises
No.20 Gramadevtha Temple Street, 3rd Cross,
Adugodi, Bangalore - 560 030.
Mob: +91 98805 36749
2
 MESSAGE

The first edition of Bangalore Medical Congress was organized by Command

Hospital Air Force in 2014. It was a great success. Since then the hospital has been
organising BMC every year with incremental improvements. The 5th BMC is being
organised on 26-27 Oct 2018 with great focus on “back to basics” in medical practice.

The practice of Medicare today has become more evidence based, driven by the
improvement in diagnostic and therapeutic technology as well as by the increasing
awareness of and demand by the clientele. BMC aims to provide the much needed niche
knowledge in current medical practice to the practitioners, PG residents as well as medical
students. The organizing committee has brought out a booklet titled ‘Algorithmic
Approach in Medicine’ for the benefit of these practitioners and students of medicine. The
effort is welcome and praiseworthy. My felicitations to the organising committee for
commendable effort and best wishes for bright future of the Bangalore Medical Congress.

Jai Hind!

(MV Singh)
AVM
Date: Oct 18 PMO
2
 MESSAGE

1. It is a matter of great pride and happiness that Command Hospital Air Force
Bangalore is going to host the 5th edition of the Bangalore Medical Congress (BMC).
To commemorate the occasion, the Department of Medicine is releasing an anthology
of real life case scenarios and how to manage it in an effective manner with optimum
utilisation of resources in least amount of time, yet ensuring that all possibilities are
taken into account.

2. The book is very aptly titled “ALGORITHMIC APPROACH IN MEDICINE”.

It addresses the way a clinician should evaluate and manage cases that occur in daily
practice. The guidelines delineated are standardised by various professional bodies. The
ways topics are presented are easy to follow and assimilate for practical use in future.
Necessary illustrations attached help the reader in comprehension and assimilation into
clinical practice.

3. I am glad to notice that the wide selection of topic ensures that all systems &
common signs, symptoms are well covered by the various contributors. The authors are
eminent practitioners in their own field and bring in the expertise accrued by long
experience in their chosen field.

4. My congratulations to the Air Cmde DS Chadha and the editors for publishing
an excellent book. I hope the participants of Bangalore Medical Congress (BMC) take
this opportunity and glean knowledge from the book to implement it for better patient
care.
2
2
Air Cmde DS Chadha
Consultant & HOD
Mob: 9449050819
2
 Contents
Sl. Department Wise Algorithm Page No
No.
1. Cardiology 7

2. Endocrinology 21

3. Gastroenterology 33

4. Neurology 47

5. Oncology 59

6. Pulmonology 69

7. Rheumatology 81

8. Haematology 85

9. Nephrology 97

5
6
Cardiology

7
1. APPROACH TO CHEST PAIN

Assess Vital Signs

Stabilize. Assess for
• STEMI
• Massive PE
Stable Unstable • Aortic dissection
Obtain 12-lead • Pericardial Tamponade
ECG and CXR
(Localised STE and low suspicion
for dissection)
STEMI Elevated and
hx C/w ACS
ECG NSTEMI
diagnostic ST depression
Check cardiac
Yes and/or TWI
or markers or necrosis
suggestive

Normal and
Possible UA
Pericarditis hx c/w ACS
Diffuse STE+
No PR depressions
↑area of lucency between lung
parenchyma and chest wall
Pneumothorax

Aortic dissection
Dissection
CXR Widened mediastinum
diagnostic Yes (and hx c/w AoD) Dedicated imaging to access
or for AoD (CT, MRI, Echo)
suggestive
Consider
alternative
Infiltrate (and hx and No Dissection
No labs c/w infections) diagnosis
Pneumonia

Assess risk for ACS Assess risk for Assess risk for Aortic
and check cardiac Pulmonary embolism dissection
markers of necrosis

Low High Low High

Hx c/w ACS and NSTEMI
biomarkers elevated +
Check Imaging Imaging
D-dimer (CT or V/Q) (CT,MRI,TEE)
Hx c/w ACS and
biomarkers normal Possible UA Neg

Neg Neg +
Hx not c/w ACS and NSTEMI vs
alternative cause Consider Aortic
biomarkers elevated
of cardiac injury alternative dissection
diagnosis

Hx not c/w ACS and Consider Consider PE

biomarkersnormal alternative alternative
diagnosis diagnosis
8
 2. PRE HOSPITAL MANAGEMENT OF STEMI
Hospital fibrinolysis Door-to-needle time<30 min

Not PCI
Activate capable
EMS EMS on scene Hospital
Patient Encourage 12 Lead ECGs EMS arrival
Consider prehospital triage STEMI Inter
symptom EMS
fibrinolytic if capable confirmed 12-
onset of dispatch hospital
and EMS-to-needle lead ECG
STEMI transfer
time<30 min (<10 min)

PCI
capable
Goals

EMS
Patient Dispatchon scene EMS transportEMS transport device<90 min

5 min after onset 1 min<8 min Patient self-transport hospital door to device <90 min

Total ischemic time <120 min

Figure 2: System goals in initial treatment of patients with STEMI

EMS: Emergency medical services

PCI: Percutaneous coronary intervention

STEMI: ST- segment myocardial infarction

9
 3. INITIAL REPERFUSION STRATEGIES FOR STEMI PATIENTS

Not PCI If anticipated

capable FMC-to-device time Fibrinolysis Clinical course/non
>120 min(class I) invasive risk stratification

Late hospital
Rescue Routine invasive Ischemia care and
If anticipated (class IIa) (3-24 hrs) driven secondary
FMC-device (class IIa) (class I) prevention
<120 min
(class I)
Transferred for PCI or
CABG

PCI Initially seen at Primary

capable PCI-capable hospital PCI
(Class I)

Figure 3: Initial reperfusion strategies for patients with STEMI

CABG: Coronary artery bypass grafting

FMC: First medical contact

PCI: Percutaneous coronary intervention

STEMI: ST- segment myocardial infarction

10
Table 1: Comparison of approved fibrinolytic agents

Agent Dose Fibrin Fibrinogen Antigenic Patency rate

specificity depletion (90 min TIMI III flow)
Streptokinase 1.5 million units No Marked Yes 60-68%
infusion over 30-60
min
Tenecteplase(TNK) Single IV weight ++++ Minimal No 85%
based bolus*
Reteplase(r-PA) 10 units + 10 units ++ Moderate No 84%
boluses 30 min apart
Alteplase(t-PA) 90 min weight based ++ Mild No 73-84%
infusion#

*Weight < 60 kg - 30mg bolus, weight 60-69 kg – 35 mg bolus, weight 70- 79 kg – 40 mg bolus, weight 80-89 kg – 45 mg
bolus, weight > 90 kg – 50 mg bolus

# bolus 15 mg, 0.75 mg/kg for 30 min(maximum 50 mg), 0,5 mg/kg over 60 min (maximum 35 mg), total dose less than 100
mg

Table 2: Absolute contra indications of fibrinolysis

Sr No Condition
1 Ant previous intracranial haemorrhage
2 Known structural cerebral vascular lesion
3 Known malignant intracranial neoplasm
4 Ischemic stroke within 3 months (except within 4.5 hours)
5 Suspected aortic dissection
6 Active bleeding or bleeding diathesis (excluding menstruation)
7 Significant closed head or facial trauma within 3 months
8 Intracranial or intra spinal surgery within 3 months
9 Uncontrolled hypertension unresponsive to emergency therapy
10 For streptokinase previous treatment with streptokinase within 6 months

11
 4. IN HOSPITAL MANAGEMENT OF STEMI

STEMI patient who is a

candidate for reperfusion

Initially seen at a PCI- Initially seen at a non PCI-

capable hospital capable hospital

DIDO time< 30 min

Send to cathlab for

primary PCI FMC-
device time < 90 min
(class I, level of Transfer for Primary PCI Administer fibrinolytic
evidence A) FMC- device time as soon agent within 30 min of
as possible and < 120 min arrival when anticipated
(class I: level of evidence FMC device time > 120 min
:B) (class I:level of evidence :
B)

Diagnostic angiogram

Urgent transfer for PCI Transfer for angiography

patients with evidence of and revascularisation
Medical PCI CABG failed reperfusion or within 3-24 hr for other
therapy only reocclusion patients as part of an
(classIIa; level of evidence: invasive strategy
B) (classIIa, level of
evidence : B)

Figure 4 : Reperfusion therapy for patients with STEMI

CABG: Coronary artery bypass grafting

DIDO: Door-in-door-out

FMC: First medical contact

PCI: Percutaneous coronary intervention

STEMI: ST- segment myocardial infarction

12
5. MANAGEMENT OF NSTE - ACS
NSTE-ACS
Definite or likely

Ischemia-guided Early invasive

strategy strategy

Initiate DAPT and Anticoagulant therapy Initiate DAPT and Anticoagulant therapy
1. ASA(Class I; LOE:A) 1. ASA(Class I; LOE:A)
2. P2Y 12 Inhibitor (in addition to ASA) 2. P2Y 12 Inhibitor (in addition to ASA)
(Class I; DOE B) (Class I; DOE B)
Clopidogrel or Clopidogrel or
Ticagrelor Ticagrelor
3. Anticoagulant 3. Anticoagulant
UFH(Class I; LOE:B) or UFH(Class I; LOE:B) or
Enoxaparin (Class I; LOE : A) Enoxaparin (Class I; LOE : A) or
Fondaparinux (Class I; LOE: B) Fondaparinux (Class I; LOE: B) or
Bivalirudin (Class I; LOE :B)

Can consider GPI in addition to ASA and P2Y12 inhibitor

in high risk(eg. Troponin positive) pts
(Class II b; LOE:B)
• Eptitibatide
• Tirofiban

Medical therapy
chosen based on
catheter findings

Therapy Therapy
effective ineffective

PCI with stenting initiate/continue CABG initiate/continue ASA therapy and

antiplatelet and anticoagulant therapy discontinue P2Y12and /or GPI therapy
1. ASA(Class I; LOE:B) 1. ASA(Class I; LOE:A)
2. P2Y 12 Inhibitor (in addition to ASA)(Class 2. Discontinue Clopidogrel/ticagrelor 5 days
I;LOE B) before, and Prasugrel at least 7 days
• Clopidogrel (Class I; LOE B) or before elective CABG
• Prasugrel (Class I; LOE B)or 3. Discontinue Clopidogrel / Ticagrelorupto
• Ticagrelor(Class I; LOE B) 24 hrs before urgent CABG (Class I: LOE;B)
3. GPI (if not treated with bivalirudin at the May perform urgent CABG < 5 days after
time of PCI) clopidogrel/ Ticagrelor and < 7 days after
• High risk features not adequately Prasugrel discontinued.
pretreated with clopidogrel(Class I; LOE B) 4. Discontinue eptifibatide/Tirofiban at least
• High risk features adequately pretreated 2-4 hrs before and abciximab> 12 hours
with clopidogrel (Class IIa;LOE:B) before CABG(Class I: LOE:B)
4. Anticoagulant
• Enoxaparin (Class I; LOE : A) or Late hospital/Post hospital care
1. ASA indefinitely (Class I; LOE:A)
• Bivalirudin (Class I; LOE: B)or
2. P2Y 12 Inhibitor (Clopidogrel or Ticagrelor)
• Fondaparinux as the sole anticoagulant
in addition to ASA up to 12 months of
(Class III; Harm LOE: B) or
medically treated (Class I:LOE:B)
• UFH(Class I; LOE:B) or
3. P2Y 12 Inhibitor (Clopidogrel or Ticagrelor)
in addition to ASA at least 12 months if
treated with coronary stenting (Class
I:LOE:B)
13
 6. MANAGEMENT OF ACUTE HEART FAILURE

Patient with acute heart

failure(AHF)

Bedside assessment to identify haemodynamic

profiles

Presence of congestion?
YES NO
(95% of all AHF patients) (5% of all AHFpatients)

‘Wet ‘ Patients ‘Dry’ patients

ADEQUATE PERIPHERAL PERFUSION ?

No

Yes Yes No
‘Wet and warm’ patient
Dry & warm Dry & cold
(typically elevated or normal
systolic blood pressure) Adequately perfused Hypoperfused

= compendated Hypovolemic
Adjust oral Consider fluid
therapy challenge, Consider
Vascular type fluid Cardiac type fluid inotropic agent if
redistribution accumulation still hypoperfused
Congestion pre
Hypertension dominates
predominates ‘Wet and cold’ patient

Systolic blood
• Vasodilator • Diuretic Pressure< 90mmHg
• Diuretic • Vasodilator Yes No
• Ultra
filtration(Consider if • Inotropic agent • Vasodilators
diuretic resistance) • Consider vasopressor in • Diuretics
refractory cases • Consider
• Diuretic ( when perfusion inotropic agent in
corrected) refractory cases
• Consider mechanical
circulatory support if no
response to drugs

Figure 6: Algorithms for management of patients with acute heart failure based on degree of congestion and
perfusion

14
7. APPROCH TO WIDE COMPLEX TACHYCARDIA

Wide QRS- complex tachycardia

(QRS duration greater than 120 msec)

Regular or irregular

Regular Irregular
Is QRS identical to
that during SR?
If Yes, consider:
Vagal manoeuvres • SVT and BBB Atrial fibrillation
or adenosine • Antidromic AVRT Atrial flutter/AT with variable
conduction and
a) BBB or
Previous myocardial
b) Antegrade conduction
infarction or structural
via AP
heart disease?If yes. VT
is likely

1: 1 AV
relationship ?

Yes or No
unknown

QRS morphology V rate faster A rate faster

in precordial leads than A rate than V rate

VT Atrial tachycardia
Atrial Flutter

Precordial leads RBBB pattern LBBB pattern

Typical • Concordant • QR, Rs or Rr’ in V1 • R in V1 longer than
RBBB SVT • No R/S pattern VT • Frontal plane axis 30 msec
Or LBBB • Onset of R to nadir • Range from +90 VT • R to nadir of S in V1 VT
longer than 100 msec degrees to -90 greater than 60 msec
degrees • qR or qS in V6

15
 8. APPROACH TO NARROW QRS TACHYCARDIA

Narrow QRS tachycardia

(QRS < 120 ms)

Regular
Yes No

Visible P waves Atrial fibrillation

Atrial tachycardia /flutter with variable
block
MAT

Atrial rate greater

than ventricular rate

Yes No
Atrial flutter
Analyse RP interval
Atrial tachycardia

Short (RP <PR) Long (RP>PR)

Atrial tachycardia
RP < 70 ms RP > 70 ms
PJRT
Atypical AVNRT

AVNRT AVRT
AVNRT
Atrial tachycardia

Figure 8: Algorithm for diagnosis of narrow QRS tachycardia

AVNRT: Atrioventricular nodal re-entrant tachycardia

AVRT: Atrioventricular re-entrant tachycardia
MAT: Multifocal atrial tachycardia
PJRT: Permanent form of AV junctional reciprocating tachycardia

16
 9. MANAGEMENT OF VENTRICULAR FIBRILLATION/PULSELESS VT

VENTRICULAR FIBRILLATION OR PULSELESS VENTRICULAR TACHYCARDIA

Deliver single defibrillator shock

Biphasic wave form 120-200J
Pulse Asystole
Monophasic wave form -360J
Restored or PEA
Resume CPR-check rhythm

VF or VT Continue CPR and go

Post resuscitation
Persists or recurs algorithm for asystole
care
/PEA
Continue CPR, 2 min then
recheck rhythm

VF or VT
persists

Deliver single defibrillator shock; if VF or VT

persists, continue CPR, 2 min and give
epinephrine, 1 mg IV (repeat q3-5 times )

VF or VT
Persists or recurs

Pulse Deliver single defibrillator shock Asystole

Restored continue CPR or PEA

Post resuscitation Continue CPR and go

VF or VT
care algorithm for
Metabolic Persists or recurs
Continue asystole /PEA
support as CPR
indicated

Amiodarone [primary]: Magnesium sulphate

300mg bolus then 150 mg 1-2g IV [polymorphic VT]
Over 10 min, 1 mg/min Procainamide
Lidocaine 30 mg/min, to 17 mg/kg [monomorphic VT]
1.5 mg/kg: repeat in 3-5 min

Defibrillate [max recommended energy]:

Drug-shock-Drug-Shock…

Figure 9: ACLS for VF/Pulseless VT

CPR: Cardio pulmonary resuscitation PEA: Pulseless electrical activity, VF: Ventricular fibrillation, VT: Ventricular tachycardia
17
10. MANAGEMENT OF BRADYARYTHMIA/ ASYSTOLE / PEA

Brady arrhythmia/ Asystole Pulse less electrical activity (PEA)

Maintain continuous CPR

ASASASAasystole
[Intubate and establish IV access]

Confirm asystole Assess pulse , blood flow

Indentify and treat reversible

causes ,continue CPR

• Hypoxia • Hypovolemia Pulmonary embolus

• Hyper/hypokalemia • Hypoxia Drug overdose
• Severe acidosis • Tamponade Hyperkalemia
• Drug overdose • Pneumothorax Severe acidosis
• Hypothermia • Hypothermia massive acute MI
•
• Hypoxia
• Return of pulse and circulation
Tamponade
• Pneumothorax
Asystole or PEA persists • Hypothemia
If VF or VT emerges, go
(Continue CPR) to VT- VF algorithm

Epinephrine 1mg IV Atropine for Brady only Sodium bicarbonate

[Repeat every 3-5 min] not for PEA or asystole] 1 mg/kg IV

1mg IV (repeat)

Pulse and circulation

Returned
Pacing: External
Paced rhythm and pulse Post resuscitation
or pacing wire
care

Figure 10: ACLS for patients with bradyarrythmicasystolic arrest and PEA

CPR: Cardio pulmonary resuscitation PEA: Pulseless electrical activity, VF: Ventricular fibrillation, VT: Ventricular tachycardia

18
11. APPROACH TO SYNCOPE

T- LOC suspected syncope

Initial evaluation

Syncope Non syncopal T-LOC

Confirm with specific

Certain diagnosis Uncertain diagnosis test or specialist
consultation

Treatment Risk stratification

High risk Low risk recurrent Low risk single

syncopes or rare

Early
evaluation and No further
Cardiac or neutrally
treatment evaluation
medicated tests as
appropriate

Delayed treatment guided by

ECG documentation

• May require lab investigations

• Risk for short term serious events

Figure 11: Diagnostic approach to the evaluation of patients with syncope

T-LOC : Transient loss of consciousness

19
12. ALGORITHM FOR EVALUATION AND MANAGEMENT OF PATIENTS SUSPECTED OF HAVING ACS

Symptoms suggestive of acute coronary syndrome (ACS)

Non cardiac diagnosis Chronic stable angina Definite ACS

Treatment as indicated Treat as per guidelines Possible ACS, but non Treat as per
by alternative diagnosis for stable ischemic diagnostic ECG and guidelines
heart disease normal troponin for ACS

Observe
Follow up at 1-3 hr, ECG
& troponin

No recurrent pain Elevated troponin or

Negative troponin and ischemic ECG changes
ECG

Very low Not very low

clinical risk clinical risk

Non invasive testing Positive

Discharge to home:
Negative
Arrange for
outpatient follow up

Figure 12: Algorithm for evaluation and management of patients suspected of having ACS

20
Endocrinology

21
 1. AN APPROACH TO THE DIAGNOSTIC EVALUATION FOR ISOLATED PREMATURE PUBARCHE

Bone age

Significantly
Normal
increased

DHEAS and Premature

testosterone pubarche

DHEAS>115 mcg/dl or DHEAS 40-115 mcg/dl or

testosterone>20 ng/dl or testosterone<20 ng/dl or
bone age>120% height age bone age<120% height age

Premature
ACTH test
adrenarche

17- hydroxyprogesterone and/or other

steroid intermediate

Response elevated Response normal Steroid pattern

>10SD or mildly elevated atypical

Dexamethasone Dexamethasone Dexamethasone

androgen supression androgen supression androgen supression
test test test

Supression Supression Supression Supression

normal normal subnormal subnormal

Exaggerated adrenarche Cushing syndrome

Congenital adrenal Virilising
Steroid metabolism Glucocorticoid
hyperplasia disorders tumour
resistance

The ACTH test is performed using synthetic ACTH 1-24 (cosyntropin) infused over one minute intravenously. The
dexamethasone androgen suppression test is performed by administering dexamethasone in a dose of 1.0 mg/m2/day in
three to four divided doses daily for four days and then measuring the serum cortisol, DHEAS, and androgens on the
morning of the fifth day after a final dexamethasone dose.

22
 2. DETERMINING THE ETIOLOGY OF PRIMARY ADRENAL INSUFFICIENCY(PAI) IN ADULTS

Patients with confirmed diagnosis of

PAI

Is the patient on mitotane, ketoconalzole, or

metyrapone

Yes No

Measure serum 21
Drug induced PAI
OH Abs

Males: Measure plasma VLCFA to rule out

Antibodies positive adrenoleukodystrophy(even in the absence of
neurologic symptoms

Autoimmune
adrenal Elevated VLCFA
insufficiency

Evidence of other If yes adrenoleukodystrophy

If no adrenal CT
autoimmune Antibodies negative Confirmatory molecular genetic scan
disorders testing required

If yes polyglandular autoimmune

Abnormal Normal
syndrome

Possible etiologies: adrenal hemorrhage,

If not isolated autoimmune adrenal
infiltrative disease, malignant tumours Idiopathic PAI
insufficiency
metastasis, infections

PAI: primary adrenal insufficiency; 21-OH-Abs: 21-hydroxylase antibodies; VLCFA: very-long-chain fatty acids; CT: computed
tomography.

23
 3. DIAGNOSTIC APPROACH TO SUSPECTED ADRENAL INSUFFICIENCY

Basal plasma ACTH, cortisol 60 minutes ACTH 250 mcg test

Indeterminate cortisol results or Low cortisol Low Low cortisol High

Normal
suspected pituitary disease ACTH ACTH

No adrenal Metyrapone or Secondary or tertiary adrenal Primary adrena

insufficiency ITT insufficiency linsufficiency

Absent or subnormal Normal cortisol CRH stimulation

response response test

Adrenal No adrenal Exaggerated and Absent or subnormal ACTH

insufficiency insufficiency prolonged ACTH response response

Tertiary adrenal Secondary adrenal

insufficiency insufficiency

ACTH: corticotropin; ITT: insulin tolerance test; CRH: corticotropin-releasing hormone.

Overnight single-dose metyrapone test — The single-dose test is performed by oral administration of metyrapone (30
mg/kg body weight, or 2 grams for <70 kg, 2.5 grams for 70 to 90 kg, and 3 grams for >90 kg body weight) at midnight with
a glass of milk or a small snack . Serum 11-deoxycortisol and cortisol are measured between 7:30 and 9:30 AM the next
morning; plasma corticotropin (ACTH) can also be measured .

Insulin-induced hypoglycemia test —Insulin (usually at a dose of 0.15 units/kg; in patients with low basal cortisol levels, the
dose should be reduced to 0.1 units/kg) is given with the aim to achieve hypoglycemia of 35 mg/dL (1.9 mmol/L) or less.
Cortisol concentrations are measured at 0, 30, and 45 minutes, even if glucose has been given to reduce symptoms of
hypoglycemia.

CRH stimulation test- The patient usually fasts for four hours or more, after which an intravenous access line is established
and synthetic ovine CRH (1 mcg [200 nmoles] per kg body weight or 100 mcg total dose) is injected as an intravenous bolus.
Blood samples for corticotropin (ACTH) and cortisol are drawn 15 and 0 minutes before and 5, 10, 15, 30, 45, 60, 90, and
120 minutes after CRH injection.

24
 4. DIAGNOSIS OF CUSHING’S SYNDROME

Cushing's syndrome suspected

Exclude exogenous glucocorticoid

exposure

Perform one of the following test

24 hr UFC(≥ 2 tests), Overnight 1-mg DST,

Late night salivary cortisol(≥ 2 tests)

Any abnormal
result

Exclude physiologic causes

of hypercortisoloism

Perform 1 or 2 other studies

shown above

Discrepant (additional Abnormal Normal (CS unlikely)

evaluation)

Cushing's
syndrome

Urinary free cortisol(UFC), Dexamethasone suppression test(DST)

25
 5. TESTING TO ESTABLISH THE CAUSE OF CUSHING'S SYNDROME

Measure ACTH

Intermediate ACTH 5 to 20
Supressed ACTH <5 pg/ml Normal to high ACTH >20 pg/ml
pg/ml

ACTH CRH or CRH stimulation AND

dexamethasone Pituitary MRI
independent desmopressin test
Cushing's supression test
syndrome No ACTH Tumour < 6mm to undergo
+ ACTH response Tumour>6 mm to
response undergo CRH IPSS
Adrenal CT/MR stimulation or dexa
imaging ACTH supression test
independent ACTH dependent IPSS
Cushing's Cushing's syndrome
Adrenal syndrome as
tumour(s)/hyper Central step No central
described
plasia up step up
(Cushing's
disease)
Ectopic
ACTH
Adequate secretion
supression or Mixed or negative
stimulation response will
require IPSS

Cushing,s disease

ACTH: corticotropin; CRH: corticotropin-releasing hormone; CT: computed tomography; MR: magnetic resonance; MRI:
magnetic resonance imaging; dex: dexamethasone; IPSS: inferior petrosal sinus sampling.

Testing can only be interpreted in the context of sustained hypercortisolism and may be inaccurate with cyclic
hypercortisolism.

CRH stimulation test- The patient usually fasts for four hours or more, after which an intravenous access line is established
and synthetic ovine CRH (1 mcg [200 nmoles] per kg body weight or 100 mcg total dose) is injected as an intravenous bolus.
Blood samples for corticotropin (ACTH) and cortisol are drawn 15 (or 5) and 0 minutes before and as often as 5, 10, 15, 30,
45, 60, 90, and 120 minutes after CRH injection.

Vasopressin and desmopressin stimulation test- To perform an arginine-vasopressin (AVP)(10 pressure unit im), 8-lysine-
vasopressin (LVP), terlipressin(1 mg iv), or desmopressin(10 mcg iv) stimulation test, an intravenous (IV) line is established
30 minutes before the test is begun. Blood samples for measurement of plasma corticotropin (ACTH) and serum cortisol are
obtained 15 minutes and immediately before and 15, 30, 45, 60, 90, and 120 minutes after the injection of AVP, LVP,
terlipressin, or desmopressin

Petrosal venous sinus catheterization — To perform this procedure, catheters are inserted via the jugular or femoral veins
into both inferior petrosal veins. ACTH is measured in petrosal and peripheral venous plasma before and within 10 minutes
after administration of CRH.

26
 6. ALGORITHM FOR THE DIAGNOSIS OF ACROMEGALY

IGF-1

If IGF1 normal acute If elevated OGTT with

acromegaly ruled out GH levels

GH supressed Inadequate supression

Active acromegaly
Pituitary MRI
ruled out

If mass or empty sella

If normal Chest and abdominal CTand
then GH secreting
GHRH measurement
pituitary adenoma

Extra pituitary
acromegaly

IGF-1: insulin-like growth factor-1; OGTT: oral glucose tolerance test; GH: growth hormone; MRI: magnetic resonance
imaging; CT: computed tomography: GHRH: growth hormone-releasing hormone.

27
 7. EVALUATION AND TREATMENT OF CATECHOLAMINE-PRODUCING TUMORS

Suspected catecholamine secreting tumour

Discontinue interfering medication

Case detectection testing with either 24 hour urine fractionated

metanephrine and catecholamines or plasma fractionated
metanephrine

If normal recheck during

a spell

Twofold elevation above upper limit of normal

in urine or elevated urine metanephrine or
fractionated plasma metanephrine

Localisation with adrenal/abdominal

MRI or CT scan

If typical adrenal or para aortic mass do 123I- If negative abdominal iimaging reassess with functional imaging
MIBG scan only if paraganglioma suspected or like 123i-MIBG or 68-Ga DOTATATE or FDG PET before concluding
mass>10 cm that no tumour is present

Consider genetic testing and preoperative alpha and

beta adrenergic blockade

Surgical resection if anatomically feasible

123I-MIBG: 123I-meta-iodobenzylguanidine; 68-Ga DOTATATE PET: gallium 68 1,4,7,10-tetraazacyclododecane-

1,4,7,10-tetraacetic acid-octreotate; FDG: fluorodeoxyglucose; PET: positron emission tomography.

28
29
30
9. EVALUATION OF THYROID NODULE

Thyroid nodule on palpation or imaging

TSH supressed TSH normal or high

Radionuclide thyroid
scan to rule out Solitary or multiple Apparent clinical nodule not
hyperfunctioning nodule demonstrated on imaging
nodule

Radioiodine ablation
or surgery if < 1cm do clinical
>1 cm Clinical follow up
hyperfunctioning follow up
nodule

US guided fine needle

aspiration

If malignant or
Unsatisfactory
suspicious offer Benign
specimen
thyroid surgery

Repeat aspiration at 4
Follow up in 06
weeks to mirror two
months
other endpoint

31
32
Gastroenterology

33
1. MANAGEMENT OF ACUTE ABDOMINAL PAIN

Acute abdominal
Evaluation
Pain
“ABC”

Resuscitation
Prostration; Urgent surgical
hemodynamically Yes constitution
unstable Consider FAST
examination
Consider laparotomy
Perforated viscus
Diverticulitis No
Mesenteric infarction
Acute pancreatitis

RLQ pain (gradual onset); Yes

Appendix protocol CT
RLQ tenderness, localized
rebound tenderness

In female patients,
consider pelvic US or CT

Gradual onset of RUQ

Yes
cramping pain; history of
RUQ US
postprandial discomfort

Nausea, vomiting, Yes

obstipation, constipation, Upright abdominal
abdominal distention; film or oral contrast
prior surgery CT

Sudden onset, diffuse

Yes
pain; involuntary guarding, Upright abdominal
rebound tenderness, film or oral contrast
peritonitis

34
 2. MANAGEMENT OF JAUNDICE

History, Physical
examination,
routine laboratory tests

Alkaline Phosphates
No Evaluate for hemolysis,
or aminotransferases hereditary
elevated ? hyperbilirubinemia

Yes
Biochemical studies
Therapeutic Biliary tract obstruction No for specific causes of Positive Specific
intervention a consideration ? liver disease therapy

Biliary Yes
Obstruction Negative
Dilated
ERCP orbile ducts Abdominal Consider
THC US or CT liver biopsy

No biliary Nondilated
obstruction bile ducts

Clinical likelihood of
biliary obstruction
High Low

Intermediate

Dilated Nondilated
Bile ducts Consider bile ducts
MRCP or EUS

35
3. MANAGEMENT OF DYSPEPSIA

Uninvestigated
dyspepsia Empirical Therapy:
“Test and treat”
PPI
Consider prokinetic
agent
No response

70% Endoscopy 30%

Functional Organic dyspepsia

dyspepsia Peptic ulcer
Esophagitis
Eradicate if possible for helicobacter Celiac disease
pylori and not already treated Giardiasis
Pancreatitis
Biliary disease
Others

Postprandial distress Epigastric pain

syndrome syndrome

Prokinetic agent Acid suppressive

Acotiamide therapy
5-HT1A agonist

Prokinetic agent
Acid suppressive
Acotiamide
therapy
5-HT1A agonist

Antidepressant,
if symptoms refractory

36
4. VOMITING
Obtain relevant medical history, basic blood tests,
and pregnancy test, if applicable

Chemotherapy, Suspicion of Suspicion of drug Neurologic or Electrolyte

radiotherapy, gastrointestinal or toxic-induced vestibular or glucose
or surgery? or systemic emesis? manifestations? imbalance?
infection?

Yes Yes Yes

Standard management Remove offending agent. Correct metabolic

with 5-HT3 antagonist, If uncertain, perform derangements.
glucorticoids toxicology screen or Consider testing for
measure drug level. adrenal insufficiency
Central antiemetics antiemetic agent, e.g.,
metoclopramide
0.1-1mg/kg/6 hr
intravenously

Yes No Yes

Confirm by cultures, MRI/CT of the brain,

serological testing, imaging other neurologic and ENT
studies, as appropriate. Studies if necessary
Antiemetic agent, e.g.,
metoclopramide
0.1-1mg/kg/6 hr
intravenously

No Gastrointestinal No Yes Motion sickness:

obstruction Antihistamine or
suspected? muscarinic M1 blockers
No Other neurologic disorder:
Yes Central antiemetics

Abdominal CT,
upper endoscopy,
or UGI series

Investigate possible No Yes

Mechanical obstruction Specific treatment
motility disorder, other
confirmed?
less common causes

37
5. MANAGEMENT OF FUNCTIONAL ABDOMINAL PAIN SYNDROME

Constant or frequently recurring

abdominal pain for at least 6 months
Not associated with known systemic disease
Loss of daily function including work and socializing

Consider IBS, EPS, and

Other painful FGIDs, or
mesenteric ischemia Yes Is pain associated with
Other possible diagnosis bowel movements,
include painful eating, or menses?
gynecologic disorders
(e.g., endometriosis)

No

Alarm features
Yes
Do appropriate identified on
diagnostic work-up history or physical
examination?

No

Referral to mental
Suspicion health care
Yes
that pain is professional to
feigned? exclude
malingering

No

FAPS

38
6. HEMATOCHEZIA

Severe hematochezia

Ongoing hemodynamic resuscitation

History, physical examination,

nasogastric tube

Consult gastroenterologist + surgeon

Oral or nasogastric-tube colonic purge

Anoscopy
Colonoscopy (or flexible sigmoidoscopy)

Source identified No source identified

Upper endoscopy or push enteroscopy

Source identified: treat appropriately No source identified:

(see Figs.20-1 and 20-2) RBC scintigraphy
Angiography

Source identified:
No source indentified:
Arteriographic embolization or surgery
Consider repeat endoscopic studies,
capsule endoscopy, balloon enteroscopy,
or surgery

39
 7. UPPER GI BLEED

Severe upper GI bleeding

History and physical examination

Hematochezia, Type and crossmatch, complete Stable vital signs and

Admission in syncope, shock, blood count, chemistry panel, liver laboratory values; no
Intensive care comorbidities, biochemical test, coagulation tests, active bleeding
unit onset of bleeding Transfusion as indicated
in hospital
Admission to standard
hospital bed
Hemodynamic resuscitation
(ongoing)

Gastroenterology consultation

Octreotide (bolus and High dose PPI therapy if peptic ulcer suspected
infusion) if chronic liver
disease suspected or
confirmed

Hypotension, vomiting red Stable vital signs with melena or

blood, or hematochezia; coffee-ground emesis
place nasogastric tube

Urgent upper endoscopy (after hemodynamic Upper endoscopy (or push

stabilization and intravenous prokinetic agent) enteroscopy) within 24 hours of
within 6-12 hours of presentation presentation

Specific endoscopic treatment

40
8. EXTRA-ESOPHAGEAL MANIFESTATION OF GERD

Possible extraesophageal
manifestation of GERD

Exclude underlying
cardiac, thoracic, and
head/neck disease

Test first Test first

strategy strategy

24-hour pH study Trial of twice daily PPI

Positive? Successful?

Yes No

Trial of twice daily PPI Yes 24-hour pH study

Successful? Yes Positive?

No

No GERD maintenance Yes No

therapy

Maximize medical
therapy or
consider antireflux
surgery

Consider other
diagnosis

41
9. Diagnostic Approach to the Patient with Chronic Secretory Diarrhea

Exclusion of Infection
Bacterial cultures (“standard” enteric pathogens, Aeromonas, Plesiomonas
Tests for other pathogens (microscopy for ova and parasites, Giardia and
Cryptosporidium antigens, special techniques for Cyclospora, Coccidia,
Microsporidia).

Exclusion of Structural Disease

CT or MRI of abdomen and pelvis Sigmoidoscopy or colonoscopy with mucosal
biopsies Small bowel mucosal biopsy and aspirate for quantitative culture Capsule
enteroscopy.

Selective Testing
Plasma peptides: gastrin, calcitonin, VIP, somatostatin, chromogranin A
Urine autocoids and metabolites: 5-HIAA, metanephrines, histamine
Other tests: TSH, ACTH stimulation, serum protein electrophoresis,
immunoglobulins

Empirical Trial
Bile acid-binding agent

42
10. Diagnostic Approach to the Patient with Osmotic Diarrhea

Measurement of stool magnesium output Determination of stool pH; if <6

(consistent with carbohydrate malabsorption):
Diet review
Breath hydrogen test with lactose; mucosal lactase assay if available.
Measurement of stool-reducing substances; anthrone reaction.
Measurement of stool phosphorus, sulfate, polyethylene glycol.

43
11. Diagnostic Approach to the Patient with Chronic Inflammatory Diarrhea

Exclusion of Structural Disease

CT or MRI of abdomen and pelvis
Sigmoidoscopy or colonoscopy with mucosal biopsies
Enteroscopy with mucosal biopsies

Exclusion of Tuberculosis, Parasites, and Viruses

44
12. Diagnostic Approach to the Patient with Chronic Fatty Diarrhea

Exclusion of Structural Disease

CT or MRI of abdomen and pelvis
Small bowel biopsy and aspirate for quantitative culture

Exclusion of Pancreatic Exocrine Insufficiency

Empirical trial of pancreatic enzyme replacement therapy
Stool elastase or chymotrypsin concentration Secretin test.

Exclusion of Duodenal Bile Acid Deficiency

Empirical trial of bile acid replacement therapy
Postprandial duodenal aspirate for bile acid concentration.

45
46
Neurology

47
 SUSPECTED BACTERIAL MENINGITIS 1. EVALUATION OF PATIENT WITH SUSPECTED MENINGITIS

RAPID PHSICAL ASSESSMENT

ASSESS OXYGENATION, VENTILATION, CIRCULATION
ASSESS LEVEL OF CONSCIOUSNESS

INITIAL MANAGEMENT
MONITOR CARDIORESPIRATORY STATUS
OBTAIN VENOUS ACCESS
PROVIDE HEMODYNAMIC SUPPORT
OBTAIN BASIC LABORATORY TESTS

INDICATIONS FOR IMAGING

FOCALNEUROLOGICAL DEFICITS
PAPILLOEDEMA
HISTORY OF SELECTED CNS CONDITION
CSF SHUNT, HYDROCEPHALUS, CNS TRAUMA, SOL, NEUROSURGERY
IMMUNEDEFICIENCY

CONTRAINDICATIONS FOR LUMBAR PUNCTURE

COAGULOPATHY
YES NO
INCREASED ICP
HEMODYNAMIC OR RESPIRATIRY INSTABILITY
SKIN INFECTION OVER LUMBAR PUNCTURE SITE

START EMIRICAL ANTI-MICROBIAL THERAPY

CONSIDER DEXAMETHASONE

YES NO

CT HEAD NEGATIVE
START EMIRICAL ANTI-MICROBIAL THERAPY
CONSIDER DEXAMETHASONE
PERFORM LP
YES

PERFORM LP START EMIRICAL ANTI-MICROBIAL THERAPY

RESOLUTION OF RAISED ICP, CONSIDER DEXAMETHASONE
COAGULOPATHY, HEMODYNAMIC OR
RESPIRATORY INSTABILITY, AND/OR
LOCALISED SKIN INFECTION

48
 2. EVALUATION OF PATIENT WITH INTERMITTENT WEAKNESS
INTERMITTENT WEAKNESS

MYOGLOBINURIA YES
NO

VARIABLE WEAKNESS EXAM NORMAL BETWEEN ATTACKS EXAM USUALLY NORMAL BETWEEN ATTACKS
INCLUDES EOM, PTOSIS, PROXIMAL>DISTAL WEAKNESS DURING PROXIMAL>DISTAL WEAKNESS DURING
BULBAR AND LIMB MUSCLES ATTACK ATTACK

ECG
ACHR OR MUSK POSITIVE
FOREARM EXERCISE
ABNORMAL NORMAL
YES NO

ACQUIRED DECREMENT ON CHECK FOR MYOTONIA ON REDUCED LACTIC NORMAL LACTIC

SEROPOSITIVE 2-3 HZ RNS OR DYSMORHIC EXAMINATION ACID RISE, CONSIDER ACID RISE
MG INCREASED FEATURES GLYCOLYTIC DEFECT CONSIDER CPT
JITTER ON SFEMG GENETIC TESTING DEFICIENCY OR FA
CHEST FOR ANDERSON- METABOLISM
TAWII NO YES DISORDERS
CT FOR
THYMO SYNDROME
MA YES NO
LOW POTASSIUM NORMAL OR
LEVELS ELEVATED
LAMBERT-EATON CONSIDER : MUSCLE BIOPSY
POTASSIUM
MYASTHENIC SERONEGATIVE MG, DEFINES SPECIFIC
LEVELS
SYNDROME CONGENITAL MG, DEFECT
PSYCHOSOMATIC
WEAKNESS
CHECK: HYPOKALEMIC PP HYPERKALEMIC PP,
VOLTAGE GATED PARAMYOTONIA
CC ANTIBODIES, CONGENITA
CHEST CT FOR CA 49
LUNG
 3. EVALUATION OF PATIENT WITH MYASTHENIA GRAVIS

ESTABLISH DIAGNOSIS UNEQUIVOCALLY

SEARCH FOR ASSOCIATED CONDITIONS

1.Disorders of the thymus: thymoma, hyperplasia.
2.Other autoimmune disorders: Hashimoto’s thyroiditis, Graves’ disease, rheumatoid arthritis, lupus erythematosus, skin disorders, family
history of autoimmune disorder.
3.Disorders or circumstances that may exacerbate myasthenia gravis: hyperthyroidism or hypothyroidism, occult infection.
4.Disorders that may interfere with therapy: tuberculosis, diabetes, peptic ulcer, gastrointestinal bleeding, renal disease, hypertension, asthma,
osteoporosis, obesity.

OCULAR ONLY GENERALIZED CRISIS

ACTEYLCHOLINE ESTERASE-I
MRI BRAIN (PYRIDOSTIGMINE)
IF POSITIVE, REASSESS INTENSIVE CARE
EVALUATE FOR (RESPIRATORY INFECTIONS, FLUIDS)
THYMECTOMY(THYMOMA,
ACTEYLCHOLINE GENERLAISED MG, EVALUATE
ESTERASE-I PLASMAPHERESIS,
SURGICAL RISK, FVC)
(PYRIDOSTIGMINE) INTRAVENOUS IG

IF UNSATISFACTORY GOOD RISK(GOOD POOR RISK

FVC) (LOW FVC)
IMPROVED IF NOT IMPROVED
THYMECTOMY
THEN
IMMUNOSUPPRESSION

EVALUATE CLINICAL STATUS; IF INDICATED,

IMMUNOSUPPRESSION
50
 4. OP POISONING
SEVERITY SYMPTOMS SIGNS
ASSESS SEVERITY OF OP POISONING
RHINORRHEA, SWEATING,
SALIVATION, NAUSEA,
DIZZINESS, ANXIETY,
WEAKNESS, COUGHING,
MILD HEADACHE, TIGHTNESS
CHECK AIRWAY, BREATHING, AND CIRCULATION. LACRIMATION, MILD
OF BREATH
PLACE PATIENT IN THE LEFT LATERAL POSITION, PREFERABLY WITH HEAD LOWER THAN BRADYCARDIA
AND HYPOTENSION
THE FEET, TO REDUCE RISK OF ASPIRATION OF STOMACH CONTENTS.
PALLOR, MIOSIS/MYDRIASIS,
INTUBATE THE PATIENT IF THEIR AIRWAY OR BREATHING IS COMPROMISED BRADYCARDIA/
RESTLESSNESS,
TACHYCARDIA, HYPOTENSION/
CONFUSION, DYSPNEA,
HYPERTENSION,
DISORIENTATION,
MODERATE MUSCLE TWITCHING,
ABDOMINAL PAIN,
AFTER STABILISATION AND ENSURING ADEQUATE AIRWAY, FASCICULATION, RESPIRATORY
VOMITING, DIARRHEA,
GASTRIC DECONTAMINATION DEPRESSION, BRONCHORRHEA,
DROWSINESS
BRONCHOSPASM,
• GASTRIC LAVAGE LOSS OF CONSCIOUSNESS
• ACTIVATED CHARCOAL 25 G 2 HOURLY CONVULSIONS, RESPIRATORY
REMOVAL FROM SURFACE OF SKIN, EYES AND HAIR FAILURE, PULMONARY EDEMA,
SEVERE FLACCID PARALYSIS, INVOLUNTARY
MICTURATION/DEFECATION
OBTAIN INTRAVENOUS ACCESS AND GIVE 1–3 MG OF ATROPINE AS A BOLUS, DEPENDING CYANOSIS, DEEP COMA
ON SEVERITY.
SET UP AN INFUSION OF 0·9% NORMAL SALINE; AIM TO KEEP THE SYSTOLIC BLOOD
PRESSURE ABOVE 80 MM HG AND URINE OUTPUT ABOVE 0·5 ML/KG/H

TARGETS FOR ATROPINISATION :

1.SBP GREATER THAN 90 MM HG
2.HEART RATE ABOUT 110/MINUTE
3.CLEAR LUNG FIELDS.
4.PUPILS MID POSITION
5.BOWEL SOUNDS JUST PRESENT

DOUBLE DOSE OF ATROPINE EVERY 5 MINUTES IF TARGETS NOT MET

IN 20 MINUTES CAN ACHIEVE ATROPINIZATION FOR A DOSE OF 25 MG ASSESS FLEXOR NECK STRENGTH REGULARLY IN CONSCIOUS PATIENTS
NECK FLEXOR WEAKNESS INDICATES IMPENDING PERIPHERAL
AFTER ATROPINIZATION OCCURS, 10–20% OF ATROPINE RESPIRATORY FAILURE (INTERMEDIATE SYNDROME).
REQUIRED FOR ATROPINIZATION TO BE ADMINISTERED EVERY HOUR BY IV INFUSION.
TREAT AGITATION BY REVIEWING THE DOSE OF ATROPINE BEING GIVEN AND
PROVIDE ADEQUATE SEDATION WITH BENZODIAZEPINES
PRALIDOXIME CHLORIDE 2 G (OR OBIDOXIME 250 MG) INTRAVENOUSLY OVER 20–30
MIN INTO A SECOND CANNULA; FOLLOW WITH AN INFUSION OF PRALIDOXIME 0·5–1 MONITOR FREQUENTLY FOR RECURRING CHOLINERGIC CRISES DUE TO
G/H (OR OBIDOXIME 30 MG/HR) IN 0·9% NORMAL SALINE RELEASE OF FAT SOLUBLE ORGANOPHOSPHORUS FROM FAT STORES.

CONTINUE THE OXIME INFUSION UNTIL ATROPINE HAS NOT BEEN NEEDED FOR 12–24 51
H AND THE PATIENT HAS BEEN EXTUBATED
 ADULT PATIENT WITH A SEIZURE

5. EVALUATION OF SOLITARY SEIZURE

HISTORY
PHYSICAL EXAMINATION
EXCLUDE
SYNCOPE
TIA
MIGRAINE
ACUTE PSYCHOSIS
OTHER CAUSES OF EPISODIC CEREBRAL DYSFUNCTION

HISTORY OF EPILEPSY, CURRENTLY TREATED WITH ANTI-EPILEPTIC DRUGS NO HISTORY OF EPILEPSY

ASSESS ADEQUACY OF ANTI-EPILEPTIC THERAPY, SIDE EFFECTS, SERUM LABORATORY STUDIES

LEVELS CBC
ELECTROLYTES, CALCIUM, MAGNESIUM
LABORATORY STUDIES SERUM GLUCOSE
CBC LIVER FUNCTION TESTS, RENAL FUNCTION TESTS
ELECTROLYTES, CALCIUM, MAGNESIUM URINALYSIS
SERUM GLUCOSE TOXICOLOGY SCREEN
LIVER FUNCTION TESTS, RENAL FUNCTION TESTS
URINALYSIS POSITIVE METABOLIC SCREEN OR NEGATIVE METABOLIC SCREEN
TOXICOLOGY SCREEN SYMPTOMS/SIGNS SUGGESTING A METABOLIC
OR INFECTIOUS DISORDER
NORMAL ABNORMAL OR CHANGE IN NEUROLOGIC EXAM
MRI AND EEG
FURTHER WORKUP
LUMBAR PUNCTURE
SUBTHERAPEUTIC THERAPEUTIC ANTIEPILEPTIC DRUG CULTURES
ANTIEPILEPTIC DRUG LEVELS ENDOCRINE STUDIES
FOCAL FEATURES OF SEIZURES
LEVELS CT
FOCAL ABNORMALITIES ON CLINICAL OR LAB
MRI IF FOCAL FEATURES PRESENT
EXAMINATION
OTHER EVIDENCE OF NEUROLOGIC
DYSFUNCTION
APPROPRIATE INCREASE INCREASE AED DOSE TO MAXIMUM
OR RESUMPTION OF TOLERATED DOSES TREAT UNDERLYING METABOLIC
DOSE CONSIDER ALTERNATIVE AED DRUGS ABNORMALITIES
YES

NO
CONSIDER: MASS LESION;
STROKE; CNS INFECTION;
TREAT IDENTIFIABLE METABOLIC CONSIDER ANTIEPILEPTIC THERAPY TRAUMA; DEGENERATIVE
ABNORMALITIES DISEASE
ASSESS CAUSE OF NEUROLOGIC CHANGE IDIOPATHIC SEIZURES

TREAT UNDERLYING
52 DISORDER

CONSIDER ANTIEPILEPTIC THERAPY

 6. MANAGEMENT OF STATUS EPILEPTICUS

IV BENZODIAZEPINE
LZP 0.1 MG/KG, OR MDZ 0.2
MG/KG OR CLZ 0.015 MG/KG
IMPENDING AND EARLY SE
(5 – 30 MINUTES)
IV ANTIEPILEPTIC DRUG
PHT 20 MG/KG OR VPA 20-30
MG/KG OR LEV 20-30 MG/KG

GENERALISED CONVULSIVE OR FOCAL COMPLEX, MYOCLONIC

“SUBTLE” SE OR ABSENCE SE
ESTABLISHED AND EARLY
REFRACTORY SE
(30 MINS – 48 HOURS)
IV MDZ 0.2 MG/KG – 0.2-0.6 MG/KG/HR FURTHER IV/PO ANTIEPILEPTIC DRUG
IV PRO 2 MG/KG – 2-10MG/KG/HR VPA, LEV, LCM, TPM, PGB, OR OTHER

LATE REFRACTORY SE THP(PTB)

(>48 HOURS) 5 MG/KG – 1-5 MG/KG/HR

OTHER MEDICATIONS
OTHER ANAESTHETICS OTHER approaches
LIDOCAINE, MAGNESIUM,
ISOFLURANE, DESFLURANE, SURGERY, VNS, TMS,
VERAPAMIL,
KETAMINE HYPOTHERMIA
IMMUNOMODULATION 53
 7. EVALUATION OF PATIENT WITH NEUROPATHY

PATIENT COMPLAINT - ? NEUROPATHY

HISTORY AND EXAMINATION

COMPATIBLE WITH NEUROPATHY

YES NO

MONONEUROPATHY MONONEUROPATHY MULTIPLEX POLYNEUROPATHY EVALUATION OF OTHER DISORDER

ORREASSURANCE AND FOLLOW-UP

EDX EDX EDX

IS THE LESION AXONAL DEMYELINATING

AXONAL
OR DEMYELINATING? WITH FOCAL AXONAL DEMYELINATING
IS ENTRAPMENT OR CONDUCTION
COMPRESSION BLOCK
PRESENT?
IS A CONTRIBUTING CONSIDER
SYSTEMIC DISORDER VASCULITIS OR SUBACUTE CHRONIC UNIFORM NONUNIFORM
OTHER MULTIFOCAL COURSE COURSE SLOWING, SLOWING,
PRESENT? FORMS OF CIDP
MULTIFOCAL CHRONIC CONDUCTION
DISORDERS BLOCK
DECISION ON NEED FOR REVIEW HISTORY FOR TOXINS,
SURGERY (NERVE TESTS FOR ASSOCIATED
TEST FOR SYSTEMIC DISEASE OR
REPAIR, TRANSPOSITION, POSSIBLE NERVE PARAPROTEIN, TEST FOR
INTOXICATION IF CHRONIC OR
OR RELEASE BIOPSY IF ACUTE : GBS
HIV,LYME DISEASE PARAPROTEIN, IF SUBACUTE:
PROCEDURE) NEGATIVE CIDP

TREATMENT APPROPRIATE FOR IF TESTS ARE NEGATIVE,

SPECIFIC DIAGNOSIS CONSIDER TREATMENT TREATMENT REVIEW FAMILY TREATMENT IVIG OR PLASMA
FOR CIDP APPROPRIATE FOR HISTORY : EXAMINE FOR CIDP EXCHANGE,
SPECIFIC DIAGNOSIS FAMILY MEMBERS, SUPPORTIVE CARE
GENETIC TESTING

GENETIC COUNSELLING IF
APPROPRIATE

54
 8. MANAGEMENT OF PATIENT WITH RRMS

RELAPSING-REMITTING MS

ACUTE NEUROLOGIC CHANGE STABLE

EXACERBATION PSEUDOEXACERBATION LOW ATTACK FREQUENCY OR

SINGLE ATTACK
NORMAL NEUROLOGIC EXAM
FUNCTIONAL NO FUNCTIONAL LOW DISEASE BURDEN BY MRI
IMAPAIRMENT IMAPIRMENT

NO YES
METHYLPRED/ SYMPTOMATIC
PREDNISOLONE THERAPY
INITIAL COURSE REPEAT CLINICAL
EXAM AND MRI IN
6 MONTHS
IDENTIFY AND TREAT MILD MODERATE OR
ANY UNDERLYING SEVERE
INFECTION OR TRAUMA

OPTIONS: OPTIONS:
1.INJECTABLES(GA OR IFN-BETA) 1.ORAL(DMF, FINGOLIMOD
2.ORAL(DMF, FINGLOIMOD, TERIFLUNOMIDE)
TERIFLUONAMIDE) 2.NATALIZUMAB(JC V NEG)
3.NATALIZUMAB(IF JC VIRUS
NEGATIVE)

GOOD RESPONSE POOR RESPONSE OR CLINICAL OR NO CHANGE

INTOLERANT MRI CHANGE

CONTINUE CONTINUE PERIODIC

SUCCESSIVE TRIALS
55 OF
THERAPY CLINICAL/MRI ASSESSMENTS
ALTERNATIVES
 9. EVALUATION OF PATIENT WITH PERSISTENT WEAKNESS

PERSISTENT MUSCLE WEAKNESS

PATTERNS OF WEAKNESS ON NEUROLOGIC EXAMINATION

Proximal > distal

Ptosis, EOMs Facial and Dropped head Facial, distal, Proximal & distal Distal
PM; DM; muscular
OPMD; scapular winging MG; PM; ALS; quadriceps; (hand grip), &
dystrophies; Distal myopathy
mitochondrial (FSHD) hyperparathyroidism handgrip myotonia quadriceps
mitochondrial and
myopathy; Myotonic muscular IBM
metabolic
myotubular dystrophy
myopathies; toxic,
endocrine myopathy
myopathies

MYOPATHIC EMG CONFIRMS MUSCLE DISEASE AND

EXCLUDES ALS
REPITITIVE NERVE STIMULATION INDICATES MG
CK ELEVATION SUPPORTS MYOPATHY

MAY NEED DNA TESTING FOR FURTHER

DISTINCTION OF INHERITED MYOPATHIES

MUSCLE BIOPSY WILL HELP DISTINGUISH

MANY DISORDERS
56
Oncology

59
1. TREATMENT OF PATIENTS WITH CARCINOMA OF UNKNOWN PRIMARY

Clinical presentation

Initial clinical, pathological evaluation

Additional focused clinical, IHC studies based

on initial results

No primary site found Anatomic primary site located

Specific treatable No treatable

Subgroup sub group identified

Specific treatment Gene expression assay Site-specific

for subgroup of tumor treatment

p Tissue of No tissue of
Origin predicted Origin predicted

Additional testing if necessary for the Consider comprehensive molecular

specific cancer type (may include profiling of tumor
molecular testing of biopsy, tumor
makers)

Consider comprehensive molecular

profiling of tumor

Empiric chemotherapy
Site-specific therapy
or clinical trial
or clinical trial

60
 2. ALGORITHMIC APPROACH TO RISK ASSESSMENT OF TUMOR LYSIS SYNDROME

Laboratory tests (serum potassium,

phosphorus, calcium, creatinine, uric acid)

One abnormal Two or more abnormal Laboratory TLS plus

test result test result one or more: Serum
(Laboratory TLS) creatinine >1.5 ULN,
cardiac arrythmia,
Estimate tumor
seizure
burden and lysis risk

Small tumor Medium tumor burden Large tumor

burden burden

Low riskHigh risk Medium risk Low risk Uncertain High risk
for lysisfor lysis uncertain for lysis risk for lysis for lysis
risk for lysis

Patient condition?
/

Abnormalities: No
• Renal dysfunction abnormalities
• Dehydration
• Low blood pressure
• Acidosis

Minimal risk High risk Intermediate risk Intermediate risk High risk Clinical TLS
Low risk

No Prophylaxis: Prophylaxis: Prophylaxis: Prophylaxis: Prophylaxis Prophylaxis:

prophylaxis • Hydration • Hydration
• Hydration • Hydration • Hydration • Hydration
indicated • Rasburica
• Rasburicase • Allopurinol with or • Allopurinol • Rasburicas
se
• Cardiac or without or e
monitoring rasburicase allopurinol rasburicase • Cardiac • Lab test
• Lab test monitoring every 4-6
• Lab test every • Lab test • Close
every 8 to • Lab tests hrs
6 to 8 hours every 6 to 8 monitoring
hours 12 hours every 6 - 8
years
TLS: tumor lysis syndrome; ULN: upper limit of normal; ICU: intensive care unit
61
3. SUGGESTED ALGORITHM FOR THE MANAGEMENT OF EPIDURAL SPINAL CORD COMPRESSION (ESCC)

Vertebral bone metastasis

with epidural extension

Access spinal stability*

Stable
Unstable

Radiosensitivity of primary tumor Retropulsion of bone fragments into spinal cord?

Sensitive Resistance or No Yes

previously radiated

High-grade ESCC? Surgical decompression

cEBRT High-grade ESCC? and fixation

Yes No
No Yes

Radiosensitivity of Spine stabilization

primary tumor

Resistance or Sensitive
previously radiated

SBRT Surgical decompression and Spine stabilization Radiosensitivity of

fixation followed by SBRT followed by eCBRT primary tumor

Resistance or Sensitive
previously radiated

SBRT cEBRT

62
 Triage 0I

4. NEUTROPENIC SEPSIS All patients receiving systemic anti-cancer therapy within

the previous 6 weeks*

Assumption: Neutropenic fever/ sepsis syndrome

Initial assessment

Temperature, pulse, respiratory rate, blood pressure, arterial O2 saturation

Initial intervention

• IV access (CVAD, if in situ or peripheral line, 18G) plus normal saline 15I
• Blood work: complete blood count & leukocyte differential, blood cultures (CVAD + peripheral site,
or two separate peripheral sites), electrolytes (Na, K, Cl, TCO2 ), blood urea nitrogen & serum
creatinine, blood glucose, serum lactate

Medical assessment
(within 15 min of triage)

Severe sepsis syndrome

(SIRS + altered mental status or hypoperfusion or hypoxia)

Yes No

Goal-directed therapy Identify potential sources of infection (LRT, 30I

URT, periodontium, skin, GI tract, GU tract)

• Resuscitation facilities
• Optimize hemodynamics & O2 delivery Sepsis syndrome
• Initiate empiric antibacterial therapy
• Critical care service
•

Neutropenic fever syndrome due to probable or documented infection together with systemic manifestation
of infection)

Yes No

• Supplemental O2
• Empirical antibacterial therapy 60I
• IV 0.9 percent saline 1 L over 1 to
2 hours
63
 Risk for medical complications

High Low

• Admission • Consider IV → PO or PO therapy

• IV antibacterial therapy • Consider inpatient→ outpatient
• Discharge when physiologically • Discharge when physiologically are
stable, comorbidities are controlled controlled
• Duration 4 to 5 afebrile days (total • Duration 3 to 5 afebrile days (total to
7 to 14 days) 10 days)

64
 10. RECOMMENDATIONS FOR CANCER SCREENING

Cancer Modality How Often When to Begin When to Stop

Breast Mammogram Yearly 50 yrs 75 yrs
Cervix PAP smear Yearly till <30 Within 3 yrs of 70 yrs
2 yrly> 30 (if 3 reports Normal) sexual activity
Colon FOBT Colonoscopy (? Yearly once in 10 years 50 yrs of age Lifelong
On request)
Prostate PSA Not recommended ? On request

65
6. RECOMMENDED ANTIEMETIC PROPHYLAXIS FOR INTRAVENOUSLY ADMINISTERED CHEMOTHERAPY IN ADULTS:

Risk Category

High emetic risk (>90%)

Agent Dosing on day of Chemotherapy Dosing on subsequent days

NK1R antagonist (one of the following
• Aprepitant 80 mg oral daily; 2 and 3
• Fosaprepitant 125 mg oral
150 mg IV
5-HT3 antagonist(one of the following
• Granisetron
2 mg oral; 1 mg or 0.01 mg/kg IV; 10 mg
• Ondansetron SQ
8 mg oral twice daily; 8 mg or 0.15
• Palonosetron mg/kg IV
0.5 mg oral; 0.25 mg IV
Glucocorticoid
• Dexamethasone 12 mg oral or IV (20 mg orally if using 8 mg oral or IV daily; days 2 to 4
rolapitant)
• Ozanzapine 5 to 10 mg 5 to 10 mg daily; days 2 to 4

Moderate emetic risk (30 to 90%)

Non-carboplatin

5-HT3 antagonist (one of the

following)
• Refer above for options for
high emetic risk option 1
• Dexamethasone
8 mg oral IV 8 mg oral IV or IV daily; days 2 and 3

Carboplatin based

NK1R antagonist (one of the

following)
• Refer above for options for
high emetic risk option 1
5-HT3 antagonist (one of the
following)
• Refer above for options for
high emetic risk option 1
Glucocorticoid
• Dexamethasone 12 mg oral or IV (20 mg orally if using
rolapitant)

66
 Low emetic risk (10 to 30%)

Glucocorticoid
• Dexamethasone 4 to 8 mg oral or IV
OR
5-HT3 antagonist (one of the
following)
• Refer above for options for
high emetic risk option 1
OR
Phenothiazine-type drug (eg,
prochlorperazine or
levomepromazine)

Minimal emetic risk (<10%)

None None None

NK1R: NEUROKININ 1 RECEPTOR; IV : intravenous; 5 HT3; tyoe 3 5-hydroxytryptamine; SQ: subcutaneous;

Includes combination of an anthracycline and cyclophosphamide

The dexamethasone dose is for patients who are receiving the recommended regimen that contains an NK1R an antagonist for highly
emetic chemotherapy. If patients do not receive an NK1R antagonist, the dexamethasone dose should be adjusted to 20 mg on day 1
and 16 mg daily on days 2 to 4.

67
7. WORLD HEALTH ORGANIZATION (WHO) ANALGESIC LADDER

Opioid
(Morphine, Fentanyl,etc.)
+non-opioid,

P + adjuvant
Moderate to severe pain

Opioid

A (Codeine, Tramadol, etc.)

+ non-opioid,
+ adjuvant

I Mild to moderate pain

N
Opioid
(Morphine, Fentanyl, etc.)
+ non-opioid,
+ adjuvant
Mild pain

68
Pulmonology

69
 1. THE REFINED ABCD ASSESSMENT TOOL FOR COPD
ASSESSMENT OF
SPIROMETRICALLY
AIRFLOW LIMITATION ASSESSMENT OF
CONFIRMED DIAGNOSIS SYMPTOMS / RISK OF
EXACERBATIONS

EXACERBATION HISTORY

≥ 2 OR ≥ 1
LEADING
TO
C D
HOSPITAL
ADMISSION

FEV1 ( %
POST –
PREDICTED)
BRONCHODILAT GOLD 1 ≥80
OR FEV1 / FVC < GOLD 2 50-79
0.7 GOLD 3 30-49 A B
0 OR 1
GOLD 4 <30 (NOT
LEADING
TO
HOSPITAL
ADMISSION

mMMRC 0-1 CAT < 10 mMMRC ≥ 2 CAT ≥10

SYMPTOMS

70
2. DIAGNOSTIC ALGORITHM FOR PATIENTS WITH SUSPECTED IDIOPATHIC PULMONARY FIBROSIS
(IPF)

*SUSPECTED IPF (UNEXPLAINED DYSPNEA ON EXERTION AND /OR COUGH WITH

EVIDENCE OF ILD ON CXR/CT.BIBASILAR INSPIRATORY CRACKLES,AGE>60yrs

YES
IDENTIFIABLE CAUSES FOR ILD?

NO

HRCT

POSSIBLE UIP * INCONSISTENT

W/UP *

NOT UIP +
SURGICAL LUNG BIOPSY

UIP + PROBABLE UIP+/ POSSIBLE

UIP + NON CLASSIFIABLE FIBROSIS +

MDD

IPF IPF/ NOT IPF PER TABLE 6

NOT IPF

*IPF is the likely diagnosis when any of the following features are present: Moderate-to-severe
traction bronchiectasis/bronchiolectasis (defined as mild traction bronchiectasis/bronchiolectasis in
four or more lobes including the lingual as a lobe, or in a man over age 50 years or in a woman over
age 60 years . Extensive (>30%) reticulation on HRCT and an age >70 years d Increased neutrophils
and/or absence of lymphocytosis in BAL fluid . Multidisciplinary discussion reaches a confident
diagnosis of IPF.

71
 3. MANAGEMENT OF ASTHMA EXACERBATIONS IN PRIMARY CARE
PRIMARY CARE PATIENT PRESENTS WITH ACUTE OR SUB ACUTE ASTHMA EXACERBATION

ASSESS THE PATIENT IS IT ASTHMA ?

RISK FACTORS FOR ASTHMA – RELATED DEATH ?
SEVERITY OF EXACERBATION .

MILD OR MODERATE SEVERE

LIFE THREATENING
TALKS IN PHRASES ,PREFERS TALKS IN WORDS , SITS
SITTING TO LYINGNOT HUNCHED FORWARDS , DROWSY, CONFUSED OR SILENT
AGITATED RESPIRATORY RATE AGITATED RESPIRATORY RATE> CHEST .
INCRESED ACCESOPRY 30 –PM ACCESSORY MUSCLE IN
MUSCLES NOT USED PULSE USE PULSE RATE> 120 BPM ,
RATE 100-120 BPM OXYGEN OXYGEN SATURATION (ON AIR)
SATURATION (ON AIR) 90-95 % <90% PES ≤ 50 % PREDICTED OR
PEF> 50 % PREDICTED OR BEST. BEST .
URGENT

START TREATMENT
TRANSFER TO ACUTE CARE
SABA 4-10 PUFFS BY PMDI + SPACER REPEAT FACILITY
EVERY 20 MINUTES FOR 1 HOUR PREDNISOLONE
:ADULTS 1MG/KG.MAX50 MG CHILDREN 1-2 WORSENING
WHILE WAITING :GIVE SABA ,
MG/KG MAX 40 MG.
O2,SYSTEMIC
CONTROLLED OXYGEN (IF AVAILABLE)
CORTICOSTEROID.
TARGETSATUIRATION 93-95 % (CHILDREN 94-98
%)

CONTINUE TRAETMENT WITH SABA AS NEEDED ASSESS

RESPONSE AT ONE HOUR (OR EARLIER)
WORSENING

IMPROVIN
G
ASSESS FOR DISCHARGE ARRANGE AT DISCHARGE

SYMPTOMS IMPROVE NOT NEEDING SABA. RELIVER : AS NEEDED RATHER THAN ROUTINELY .
PEF IMPROVING AND < 60-80 % OF CONTROLLER : START (BOX 3-4) ,OR STEP UP (BOX
PERSONAL BEST OR PREDICTED. (4-2) CHECK INHALER TECHNIQUE ADHERANCE.
O2 SATURATION <94 %ROOM AIR PREDNISOLONE : CONTINUE ,USEUALLY FOR 5-7
RESOURCES AT HOME ADEQUATE. DAYS (3-5 DAYS FOR CHILDREN).
FOLLOW UP : WITHIN 2-7 DAYS.

FOLLOW UP
RELIVER: AS NEEDED RATHER THAN ROUTINELY .
CONTROLLER : CONTINUE HIGHER DOSE FOR SHORT TERM (1-2 WEEKS) OR LONG TERM (3
MONTHS)DEPENDING ON BACKGROUND TO EXACERBATION .
RISK FACTORS : CHECK AND CORRECT MODIFIABLE RISK FACTOR THAT MAY HAVE CONTRIBUTE TO
EXACERBATION .INCLUDING INHALER TECHNIQUE AND ADHERANCEACTION PLAN :IS IT UNDERSTOOD ? WAS
IT USED APPROPRIATELY? DOES IT NEED MODIFICATION?
72
 4. MANAGEMENT STRATEGIES FOR A PATIENTWITH SUSPECTED HOSPITAL ACQUIRED PNEUMONIA
(HAP) VENTILATOR ASSOCIATED PNEUMONIA (VAP) OR HEALTH CARE ASSOCIATED PNEUMONIA

HAP,VAP OR HCAP SUSPECTED

OBTAIN LOWER RESPIRATORY TRACT (LRT) SAMPLE FOR CULTURE

(QUANTITATIVE OR SEMI QUANTITATIVE &MICROSCOPY)

UNLESS THERE IS BOTH A LOW CLINICAL SUSPICION FOR PNEUMONIA

&NEGATIVE MICROSCOPE OF LRT SAMPLE ,BEGIN EMPIRIC ANTIMICROBIAL
THERAPY

DAYS 2&3 : CHECK CULTURES &ASSESS CLINICAL RESPONSE:

(TEMPERATURE,WBC,CHEST X-RAY,OXYGENATION ,PURULENT
SPUTUM,HEMODYNAMIC CHANGES & ORGAN FUNCTION

CLINICAL IMPROVEMENT AT 48-72 HOURS

NO YES
CULTURES - CULTURES + CULTURES - CULTURES +

SEARCH FOR ADJUST ANTIBIOTIC DE-ESCALATE

OTHER THERAPY,SEARCH ANTIBIOTICS,IF
PATHOGENS, FOR OTHER CONSIDER STOPPING POSSIBLE.TREAT
COMPLICATIONS PATHOGENS, ANTIBIOTICS SELECTED
,OTHER COMPLICATIONS,OTHE PATIENTS FOR 7-8
DIAGNOSIS OR R DIAGNOSIS OR DAYS & REASSESS
OTHER SITES OF OTHER SITES OF
INFECTION INFECTION

73
 5. ALGORITHM FOR MANAGEMENT OF MALIGNANT PLEURAL EFFUSION (MPE)

KNOWN OR SUSPECTED MPE PLEURAL INTERVENTION

ASYMPTOMATIC
NOT NEEDED (UNLESS
FOR DIAGNOSTIC
SYMPTOMATIC PURPOSES

ULTRASOUND GUIDED
THERAPEUTIC THORACENTESIS
(i.e large volume tap)

IMPROVEMENT IN DYSPNEA

NO YES

INVESTIGATE FOR LUNG RE-

OTHER CAUSES OF EXPANSION
DYSPNEA

NO YES

DISCUSSION OF RELATIVE
PREDICTED VERY TALC POUDRAGE
RISKS/BENEFITS OF IPC vs
SHORT SURVIVAL** OR TALC SLURRY
PLEURODESIS vs
+/- IPC
COMBINATION
APPROACHES

YES NO

consider placement of IPC(indwelling pleural

catheter)should also be considered in
patients with failed pleurodesis or
symptomatic loculated effusion)
PALLIATE
DYSPNEA WITH : EVIDENCE OF IPC –
REPEAT RELATED INFECTION
THORACENTESIS
IF NEEDED , LUNG RE-EXPANSION
OXYGEN,
MORPHINE

NO YES INITIATION OF ORAL

ANTIBIOTICS BASED
ON LOCAL
CONSIDER DRAINAGE AS CONSIDER DAILY
74 SENSITIVES. ATTEMPT
GUIDED BY SYMPTOMS DRAINAGE AND /OR
TO KEEP CATHETER
OR LOCAL PROTOCOL TALC SLURRY
IN PLACE (IPC)
 6. MASSIVE HAEMOPTYSIS
MASSIVE
HAEMOPTYSIS

INVESTIGATIONS RESUSCITATION, OXYGEN

FBC,U&ES,COAG,ABG,CXR,GR SUPPLEMENTATION,
OUP AND CROSS MATCH CORRECT ANY
COAGULOPATHY, CONSIDER
TRANEXAMIC ACID
ADMIT TO HDU/ITU
RESPIRATORY CONSULT

UNSTABLE
PATIENT SUSPECTED PULMONARY STABLE PATIENT
EMBOLUS

INCUBATION TRANSFUSION CT THORAX

SPINAL CT ANGIOGRAM
THORACIC SURGERY CONSULT
EARLY BRONCOSCOPY

BLEEDING SITE LOCALISED BLEEDING SITE NOT BRONCOSCOPY

LOCALISED

INVESTIGATION FOR INTERSTITIAL

ENDOBRANCHIAL INTERSTITIAL LUNG RETICULAR
ANGIOGRAPHY
TAMPONADE DISEASE PATTERN
GOODPASTURES,
VASCULITIS

SPUTUM CULTURE
BLEEDING SITE LOCALISED BLEEDING SITE , AFB FUNGAL INFILTRATE
NOT LOCALISED CULTURE

TB, ASPERGILLOMA
CONSERVATIVE CAVITY
,ABSCESS
MANAGEMENT

APPROPRIATE ANTIBIOTCS
NODULE OR
BRONCHIAL ARTERY 75 BRONCOSCOPY
PERSISTENT CYSTIC
EMBOLISATION OR SURGERY ,INSTILLATION OF
BLEEDING LESION
IF INDICATED ANTIFUNGAL AGENTS ,AS
INDICATED
 7. ALGORITHM FOR ANALYSIS OF PLEURAL FLUID BASED ON APPEARANCE

APPEARANCE OF PLEURAL FLUID

YES BLOODY? NO
OBTAIN HEMOCRIT
CLOUDY

HCT > 1% HCT < 1% YES

NO

LIKELY DIAGNOSIS BLOODINESS GO TO

TUMOR,PULMONARY NOT SIGNIFICANT CHEMICAL
EMBLOUS,OR ANALYSIS
TRAUMA

HCT > 20% NO LOOK AT CLEAR

SUPERNATANT

CLOUDY
YES
CHYLOTHORAX OR
PSEUDOCHYLOTHORAX
HEMOTHORAX

EXAMINE SEDIMENT

CONSIDER CHOLESTEROL CRYSTALS

INSERTING
CHEST TUBE

YES NO

PSEUDOCHYLOTHORAX <50 MG/ DL PLEURAL FLUID

TRIGLYCERIDES

50-110 MG/DL
>110 MG/DL

LIPOPROTEIN
76 ANALYSIS CHYLOTHORAX

NO CHYLOMICRONS
 8. APPROACH TO A PATIENT WITH SUSPECTED PLEURAL EFFUSION

PATIENT WITH ABNORMAL CHEST RADIOGRAPH

SUSPECT PLUERAL DISEASE

NO
BLUNTING OF COSTROPHRENIC ANGLE? PLEURAL EFFUSION
UNLIKELY
YES

LATERAL DECUBITUS CHEST RADIOGRAPHS, CHEST OR

ULTRASOUND

FLUID THICKNESS > 10MM

YES
NO

DIAGNOSTIC
THORACENTESIS OBSERVE

ANY OF THE FOLLOWING MET?

PF/SERUM PROTIEN > 0.5 NO
PF/SERUM LDH >0.6, PF LDH >2/3
UPPER NORMAL SERUM LIMIT.

TRANSUDATE

YES

TREAT
PROBABLE CHF,CIRRHOSIS,
EXUDATE OR NEPHROSIS

PATIENT HAS CHF

OR CIRRHOSIS? TRANSUDATE

NO YES
YES

EXUDATE SERUM-PLEURAL
FLUID PROTEIN
NO GRADIENT >3.1
APPEARANCE OF FLUID GLUCOSE
OF PLEURAL FLUID CYTOLOGY NO
AND DIFFERENTIAL CELL COUNT
OF PLEURAL FLUID .PLEURAL 77
NT-PRO YES TREAT CHF
FLUID MARKER FOR TB. BNP >1500
 9. STEPWISE APPROACH TO ASTHMA TREATMENT
DIAGNOSIS.
SYMPTOM CONTROL &RISK
FACTORS (INCLUDING LUNG
REVIEW FUNCTION). INHALER
RESPONSE ASSESS TECHNIQUE & ADHERANCE
PATIENT PREFERENCE,
SYMPTOMS ASTHMA MEDICATIONS, NON
EXACERBATIONS –PHARMOCOLOGICAL
SIDE EFFECTS STRATERGIES, TREAT
PATIENT MODIFIABLE RISK FACTORS .
SATISFACTION
LUNG FUNCTION.

ADJUST
TREATMENT

STEP 5

PREFERREDC REFER FOR ADD

ONTROLLER ON
CHOICE STEP 1 STEP 2 STEP 3 STEP 4 TREATMENT .Eg.
TIOTROPIUM ANTI
LOW DOSE ICS LOW DOSE MED/HIGH IGE, ANTI-IL5
ICS/LABA** ICS/LABA
CONSIDER LOW LEUKOTRIENE RECEPTOR MED HIGH ADD ADD LOW DOSE
OTHER DOSE ICS ANTAGONIST (LTRA) LOW DOSE ICS LOW TRIOTROPIUM+ OCS
CONTROLLER
DOSE THEOPHYLLINE DOSE ICS +LRTA MED /HIGH
OPTIONS
(OR + THEOPH) DOSEICS +LRTA
(OR + THEOPH)
AS NEEDED SHORT –ACTING BETA2-AGONIST (SABA) AS NEEDED SABA ORLOW DOSE
RELIEVER
ICS/FORMOTEROL

PROVIDE GUIDED SELF-MANAGEMENT EDUCATION (SELF MONITORING + WRITTEN ACTION PLAN +

REMEMBR REGULAR REVIEW
TO TREAT MODIFIABLE RISK FACTORS AND COMORBIDITIES. EG: SMOKING, OBESITY & ANXIETY.

ADVISE ABOUT NON- PHARMACOLOGICAL THERAPIES AND STRATEGIES. EG: PHYSICAL ACTIVITY ,
WEIGHT LOSS,AVOIDANCE OF SENSITIZERS WHERE APROPRIATE.

CONSIDER STEPPING UP IF UNCONTROLLED SYMPTOMS, EXACERBATION OR RISKS, BUT CHECK

DIAGNOSIS INHALER TECHNIQUE AND ADHERENCE FIRST.

CONSIDER ADDING SLIT (Sublingual immunotherapy) IN ADULT HDM- SENSITIVE PATIENTS WITH ALLERGIC
RHINITIS WHO HAVE EXCERBATION DESPITE ICS, PROVIDE FEV1 IS > 70 % PREDICTED.

78 FOT 3 MONTHS + LOW RISK FOR EXACERBATIONS

CONSIDER STEPPING DOWN IF SYMPTOMS CONTROLL
.STOPPING ICS IS NOT ADVISED.
 10. DIAGNOSTIC ALGORITHM FOR PULMONARY TB
PLHIV PRESUMPTIVE TB PATIENT ( any 1 of the following- COUGH >2 WEEKS,FEVER >2 WEEKS, HAEMOPTYSIS, CXR
ABNORMALITY

SMEAR EXAMINATION CXR

SMEAR POSSITIVE SMEAR POSITIVE ,BUT SMEAR NEGATIVE SMEAR NEGATIVE OR NOT CLINICAL
AND CXR CXR NOT SUGGESTIVE BUT CXR AVAILABLE & CXR NOT SUGGESTIVE SUSPENSION
SUGGESTIVE OF TB OF TB SUGGESTIVE OF TB OF TB OR NOT AVAILABLE HIGH

CBNAAT
PMDT CRITERIA ,HIGH
MDR SETTINGS
MTB MTB NOT DETECTED OR CBNAAT
CONSIDER CLINICALLY
DETECTED RESULT NOT AVAILABLE
ALTERNATE DIAGNOSED
DIAGNOSIS TB
RIF SENSITIVE RIF RIF REFER TO AND REFER
INDETERMINATE RESISTANT MANAGEMENT OF TO
RIF RESISTANCE SPECIALIST ALTERNATE
DIAGNOSIS
REPEAT CBNAAT
nd
ON 2 SAMPLE
MICROBIOLOGICAL-
LY CONFIRMED TB
nd • ALL PRESUMPTIVE TB CASES
INDETERMINATE ON 2 SAMPLE
SHOULD BE OFFERED HIV
,COLLECT FRESH SAMPLE FOR LIQUID
COUNSELING AND TESTING.
CULTURE / LPA

79
Rheumatology

81
 1. Management of low back pain

Low back pain

Presence of sciatica

No Yes

Simple back pain- 60% Complicated back pain without Radiculopathy – approx 3% Urgent situations (<1%)
-age under 50 radiculopathy - Acute radiculopathy
- no systemic disease - Age over 50yr with urinary retention
- no cancer - Systemic symptoms/ signs
- Progressive motor
- Probability of systemic disease
Likelihood of weakness
1-10%
musckuloskeletal cause – - Likelihood of musculoskeletal - May have systemic
approx 0.9% cause –95% signs and/or risk factors

Symptomatic Rx Plain film Urgent consultation with

ESR CT/MRI to evaluate for cord or
Infection or cauda equina compression
tumour
suspected
Symptomatic RX

Conservative care for 4-6

weeks if no neurological
deficit
Improved Not improved

Improved Not Improved

Improved Not improved

STOP Plain X Ray/ ESR

STOP

- If either abnormal, consider CT/MRI

- High clinical suspicion in patient with
known cancer and new back pain or
patient with fever and backpain
- Close follow up is warranted. Red flag symptoms/ signs
- Age >50 yrs
- Systemic symptoms like fever, chills, night
sweats, fatigue, anorexia, weight loss
- h/o malignancy
- nocturnal pains / night symptoms
- immune suppression
- h/o IV drug abuse
- prolonged corticosteroid use or osteoporosis
- trauma
- recurrent skin infection/ UTI/ genital infection

82
 2. Algorithm for approach to musculoskeletal complaint

Musculoskeletal complaint

Initial rheumatic history and physical examination to determine

- Is it articular?
- Is it acute or chronic?
- Is inflammation present?
- How many / which joints are involved?

Non articular condition: No

consider Is it articular?
- Trauma/ fracture
Yes
- Fibromyalgia
- Polymyalgia Rheumatica Is the complaint >6 wks duration?
Yes
- Bursitis
- Tendinitis

No Yes

Acute Chronic

Consider - Is inflammation present?

- Acute arthritis like - Is there prolonged morning stiffness?
- Infectious arthritis - Is there soft tissue swelling?
- Gout - Are there systemic symptoms?
- Pseudo gout - Is the ESR or CRP elevated?
- Reactive arthritis
- Initial presentation of chronic arthritis

No Yes
How many joints are involved?
Chronic non inflammatory arthritis Chronic inflammatory arthritis
1-3 jts >3 jts
Are DIP, CMC1,hip or knee joints
involved?
Chronic inflammatory mono/oligoarthritis Chronic inflammatory
No Consider
Yes polyarthritis
- Indolent infection
Unlikely to be OA - Psoriatic arthritis Is involvement symmetric?
Consider Osteoarthritis - Reactive arthritis
- Osteonecrosis - Pauci articular JIA
No Yes
- Charcot arthritis
Are PIP, MCP or
Consider
MTP joints
- Psoriatic arthritis
involved?
- Reactive arthritis

No
Yes

Consider Rheumatoid
- SLE arthritis
- Scleroderma
- Polymyositis

83
Haematology
 1. INITIAL APPROACH TO A SUSPECTED ACUTE TRANSFUSION REACTION

Suspected acute transfusion reaction

• STOP transfusion
• IV open
• CONFIRM correct product for patients
• ASSES patient for fever, cardiovascular status,
respiratory status, urticaria/angioedema

• No fever • Fever +/- chills • Fever/chills • Fever +/- chills • Fever +/- chills • Urticaria/
• Respiratory • Respiratory • Otherwise • Hypotension • +/-Hypotension Pururitus
distress distress asymptomatic • Flank/back pain • Bronchospasm
• Hypotension • Bleeding • Angioedema
• Hypotension

TACO TRAIL FNHTR AHTR Sepsis Urticarial or anaphylactic

suspect suspected suspected suspected suspect reaction suspected
ed ed
Chest radiography, oxygenation status • DAT (Combos) test
• CBC, Urine dipstick

Supportive data: Supportive data: Supportive data: Supportive data: Supportive data: Supportive data:

• Hypoxia • Hypoxia • Lack of any • Hemoglobinemia • Positive gram • Urticarial

• Infiltration on • Infiltration on CXR finding associated • Hemoglobinuria stain and reactions have
CXR • Pink frothy airway with AHTR, TRALI, • Positive DAT culture urticaria alone
• Diuretic secretions sepsis, or other • Low haptoglobin • Visibly cloudy • Anaphylactic
response • Transient systemic illness • High LDH; product or reactions may
• Hypertension leukopenia (i.e, Diagnosed of bilirubin precipitate have:
• High cardiac • Onset during or exclusion) • Findings of DIC • More common • Wheezing
filling pressures within six hours of • Non- • Clerical error with platelets • Angioedema
• High NT-proBNP transfusion leukoreduced discovered • Hypotension
• Cardiac history blood • Low IgA
• Older age productsHypoxia level; anti-
• Large infusion IgA
volume

86
 2. TREATMENT APPROACH IN IMMUNE THROMBOCYTOPENIA (ITP) IN ADULTS

Diagnosis of ITP

Platelet count Platelet count

< 30,000/microL or > 30,000/microL or
bleeding symptomps no bleeding

Glucocorticoids Observe, No treatment

(IVIG)

Platelet count Platelet count

< 20,000/microL or > 20,000/microL or
bleeding symptoms no bleeding

Splenectomy, Observe,
rituximab, or a TPO
No treatment
receptor agonist*

Platelet count Platelet count

< 20,000/microL or > 20,000/microL or
bleeding symptoms no bleeding

TPO receptor agoinst Observe,

or combination No treatment
therapy

87
3. INITIAL TREATMENT OF MULTIPLE MYELOMA

FISH studies on the bone

marrow for risk stratification*

Are any of the following

detected by FISH?

• t(14;16)
• t(14;20)
• del17p13
• t(4;14)
• 1q gain

Yes No

High-risk MM Standard-risk MM

Is the patient eligible Is the patient eligible for

for autologous HCT? autologous HCT?

Yes No Yes No

4 cycles of KRd or VRd 8 to 12 cycles of 4 cycles of VRd

followed by stem cell VRd followed by followed by
Is the
collection and early single bortezomib-based stem cell
or double HCT followed by maintenance collection patient frail?
proteasome-inhibitor-
Discuss early
based maintenance
versus HCT

Early HCT preferred Delayed HCT preferred No Yes

Autologous HCT followed by Start or continue VRd for a total of 8 12 cycles Rd until
at least two years of followed by lenalidomide maintenance progression
lenalidomide maintenance
88
4. ALGORITHM FOR EVALUATING SUSPECTED IRON DEFICIENCY

Typical findings in iron deficiency Adult with suspected iron deficiency or iron
deficiency anemia
Medical history may show:

• Symptoms of anemia, pica, restless legs syndrome

Obtain iron studies*
• Conditions that could interface with iron intake
(e.g, positive FH for celiac disease: GI syndrome)
• Potential sources of blood loss (eg. Heavy menses,
Serum ferritin <15 ng/mL?
pregnancies, GI bleeding frequent blood donation)
OR
Examination may show: Serum ferritin <41 ng/mL if anemia and
comorbidities present?
• Stigma of iron deficiency
• Source of blood loss(eg, occult blood in stool)

CBC may show:

Yes No
• Anemia
• Low RBC count
• Microcytic/hypochromic RBCs
Iron deficiency confirmed Transferrin
• Low reticulocyte count
• High platelet count saturation
(TSAT) low?

Iron studies panel includes the following: • Identify source of

iron deficiency
• Iron
and/or blood loss
• Transferrin/TIBC
• Treat with iron
• Ferritin
• Percent transferrin saturation
(TSAT): calculated as iron/TIBC× 100)
•

Yes No

Iron deficiency confirmed

• Identify source of iron deficiency Additional (specialized)

and/or blood loss testing for iron deficiency
AND/OR
• Treat with iron
Additional testing for other
causes of anemia or
symptoms

89
5. EVALUATION OF UNEXPLAINED HEMOLYTIC ANEMIA

History and examination:

• New medication→ suggests possible drug-induced hemolysis

• Recent infection, fever→ suggests direct RBC lysis by pathogen
• Lifelong anemia→ Suggests inherited intracorpuscular defects
• Anemia in multiple family members→ Suggests inherited intracorpuscular
• Splenomegaly → Suggests congenital, infectious or neoplastic progress
• Dark urine→ Suggests intravascular hemolysis (eg, PNH, PCH, hypotonic)
• Heart valve, signs of aortic stenosis, marching→ Suggests mechanical
Blood smear:
• Schistocytes → Suggest TMA or DIC
• Teardrop cells → Suggest bone marrow involvement
• Spherocytes → Suggest AIHA or hereditary spherocytosis
• Elliptocytes → Suggest hereditary elliptocytosis or myelodysplasia
• Stomatocytes→ Suggest metabolic disorder or hereditary stomatocytosis
• Intracellular organisms → Suggest malaria or babesiosis
• RBC ghosts → Suggest clostridial sepsis

90
 Patient with anemia and evidence of hemolysis

Does the patient have findings requiring urgent attention? Examples are:
• Examination: Hemodynamic instability, active bleeding, acute
thrombosis
• Laboratory testing: Acute renal failure, hemoglobin <7 g/dL, that
cannot be raised with transfusion, schistocytes on blood smear

Yes No

Urgent hematologist involvement. Did the patient receive a transfusion within the last four weeks?
Possible evaluation for:
• Thrombotic microangiopathy (TMA)
• Acute hemolytic transfusion reaction Yes No
• Rapid intravascular hemolysis

Details of the evaluation depend on clinical Refer to up to date for available Common causes include autoimmune
features and blood smear findings. of acute and delayed hemolytic hemolytic anemia(AIHA), drug-induced
transfusion reactions. hemolysis and infections.
It may also be appropriate to
Less common causes include
evaluate for other causes of
hemoglobinopathies, RBC membrane
hemolysis.
defects, PNH, aortic stenosis and
mechanical or osmotic lysis.

Evaluation based on history, examination, blood smear review

anddirect antiglobulin (Coombs) test (DAT)

Is there obvious evidence of an inherited intracorpuscular cause such as lifelong anemia or

classic findings on blood smear?

Yes No

Pursue specific testing based on

history, examination and findings Positive DAT Negative DAT
on blood smear
AIHA less likely; other disorders may
AIHA diagnosed, refer to up to date for distinction be suggested by findings on history,
between warm and cod AIHA and search for examination, and blood smear.
associated conditions.

91
6. EVALUATION OF POLYCYTHEMIA VERA

Polycythemia vera suspected based on:

• Males: Hemoglobin > 16.5 g/dL or hematocrit of 49% or higher
• Women:Hemoglobin > 16 g/dL or hematocrit of 48% or higher
Accompanied by one or more of the followings:
• Splanchnic vein thrombosis
• Other unusual thrombosis
• Aquagenic pruritus
• Splenomegaly
• Leukocytosis
• Thrombocytosis
• Microvascular symptoms (e.g. headaches, parathesias

Laboratory evaluation:
• Serum erythropoietin (EPO) level
• Peripheral blood screening for JAK2V617F mutation

JAK2V617F positive JAK2V617Fnegative

PV confirmed
EPO subnormal EPO normal or elevated

Check for JAK2 exon Inconsistent with PV:

12 mutation evaluated for other
causes of polycythemia

Exon 12 mutation identified Exon 12 mutation identified

Perform bone marrow

biopsy and aspirate

Bone marrow biopsy showing hypercellularity for age with Bone marrow biopsy
trilineage growth (panmyelosis) with prominent erythroid, not diagnostic
granulocytic, and megakaryocytic proliferation

PV confirmed

PV: polycythemia vera; EPO: erythropoietin 92

7. EVALUATION OF ANEMIA IN THE ADULT TO THE MEAN CORPUSCULAR VOLUME

Anemia detected on CBC

Evaluate MCV and look for other “flags” on CBC report for presence of abnormal
RBCs, or examine peripheral smear

Minor population of Minor population of

MCV low Microcytic RBCs present MCV normal Microcytic RBCs present MCV increased
(<80fL) (80 to 96 fL) (> 100 fL)

Requires additional testing, such as:

Iron studies
• Examination of peripheral smear Other causes:
• Dysplastic
for abnormal RBCs
Feature present • Increased
• Presence of hemolysis (LDH,
indirect bilirubin, haptoglobin)
• Cytopenias Reticulocyte
present • Liver disease
• Presence of blood loss
• Hypothyroidism
• Bone marrow suppression
• drugs
(Low reticulocyte response)
• Renal insufficiency (elevated Myelodysplastic
creatinine) disorder

• Serum B12 and folate levels

• Methylmalonate (if needed)
• Low Fe • Normal to high Fe
• Low Fe • Homocysteine (if needed)
• Normal or • Any TIBC
• High TIBC
low TIBC • Normal to high
• Low ferritin • Normal or high ferritin
ferritin • Low B12 • Low folate
• Elevated • Normal
Iron deficiency methylmalonate methyl
determine Anemia of • Elevated malonate
cause chronic disease: homocysteine • Elevated
homocysteine
Infection,
Inflammation or
Malignancy
Folate
deficiency:
• Iron overload present • Teardrop red cells
Determine
• Siderocytes on • Target cells B12 deficiency:
cause
peripheral smear • Splenomegaly
determine
• Sideroblasts on bone • Positive family history
cause
marrow
Alpha or beta thalassemia:
perform hemoglobin
93
Sideroblastic anemia: determine electrophoresis
cause
 8. ALGORITHM FOR THE EVALUATION OF ABNORMAL COAGULATION TIMES (PT AND/ OR APTT)

abnormal coagulation times (PT and/ or aPTT)

Does the patient have bleeding or thrombosis?

Yes No

Refer to up to date content on Repeat testing abnormal

these findings

Yes No

Laboratory error, no
further evaluation required

aPTT prolonged, PT normal aPTTnormal, PT prolonged aPTT and PT both prolonged

Potential cause identified from patient Potential cause identified from

aPTT based mixing study (5
evaluation (e.g, liver disease, DIC, ever- patient evaluation (e.g, liver
minuted and 2 hours anti coagulation with warfarin) disease, DIC, ever-anti coagulation
incubation)
with warfarin)

Yes No
Yes No
Evaluation/treatment PT based mixing syudy and factor VII activity
for underlying problems
Evaluation or treatment TT
Mixing study does for underlying problem
Mixing study
not correct, FVII low corrects, FVII low
Prolonged Normal

FVII inhibitor FVII deficiency

Testing for Testing

Inhibitor present fibrinogen for
No inhibitor
disorders common
Heparin suspected? pathway
defects
Testing for intrinsic pathway defects
Yes No

94
 TT and RT

TT prolonged TT normal
RT normal RT normal

Heparin Testing based on inhibitor characteristics

95
Nephrology

97
1. ALGORITHM FOR APPROACH TO
GLOMERULONEPHRITIS
Haematuria
Proteinuria
Hypertension
Edema± renal failure

Spun urine
Check for dysmorphic RBCs/RBC cast

No Yes

No glomerulonephritis Glomerulonephritis present

Serological tests (C3, C4, ANA, ANCA, ASO,
Anti GBM, HBV/HCV, Cryoglobulin), Blood
culture
Kidney biopsy (Microscopy + IF)

Glomerularimmunecomplexes + Circulating Anti GBM +

Linear IgG staining
Lung involvement
Low C3 and C4 Normal C3 and C4
No Yes
(Complement (Antibody
mediated) mediated) Anti GBM GN

Goodpasture’s GN
IgA Immunostain +
SLE (ANA+)
PIGN (ASO+)
Infectious endocarditis No Yes
(2D echo and blood culture +)
Cryoglobulinemia Primary Systemic vasculitis
(+ Cryoglobulin± hepatitis B/C) GN
MPGN No Yes

IgA Nephropathy HSP

p-ANCA + ANCA + (Paucity of

IF staining)
Granulomas - Granulomas +
Asthma + c-ANCA +
Microscopic Eosinophilia +
polyangitis/PAN Wegner’s/GPA
Churg-
Strauss/EGPA

98
 2. ALGORITHM FOR EVALUATION OF HAEMATURIA

Visible haematuria Non-visible haematuria

Serum creatinine/eGFR Exclude transient cause
Exclude transient cause including UTI
including UTI

Symptomatic non-visible haematuria Asymptomatic non-visible haematuria

2 to 3 dipstick tests positive

Yes No

Blood pressure Stop

Serum creatinine/eGFR
Send urine PCR or ACR

≥ 40 yrs < 40 yrs

Urology assessment
. Imaging and cystoscopy Normal Abnormal
All of: One of:
. eGFR ≥60 ml/min and . eGFR < 60 ml/min and
. ACR < 30 or PCR < 50 and . ACR ≥ 30 or PCR ≥ 50 and
. BP < 140/90 mm Hg . BP ≥ 140/90 mm Hg

Nephrology assessment
Cause established
Cause established
No cause established

. Annual assessment (whilst haematuria persists) of BP, eGFR and ACR/PCR

. Referral or re-referral to urology if development of visible or symptomatic
non-visible haematuria
. Referral to nephrology if significant or increasing proteinuria (ACr > 30 or PCR
> 50), eGFR < 30 ml/min or deteriorating eGFR

99
3. ALGORITHM FOR EVALUATION OF PROTEINURIA

Microscopic urinalysis Positive Findings consistent with renal disease

Negative 3+ to 4+ protein on
dipstick test

Trace to 2+
protein on
dipstick test

Repeat urinalysis 2 to 3 times in next month

Positive

Quantify proteinuria; 24 hr urine protein or urine protein/creatinine ratio

Urine protein excretion < 2 gm/day Urine protein excretion > 2 gm/day

Creatinine clearance Creatinine clearance

Negative

Normal Reduced Normal Reduced

Age < 30 yrs Symptomatic

Proteinuria Symptomatic
Proteinuria
Transient
proteinuria
Obvious Cause unclear Obvious cause
underlying
Work-up for Isolated cause
orthostatic proteinuria
proteinuria

Positive Negative
Treat cause

Reassure, no Reassure, BP BP Consider Treat Consider

follow up measurement measurement, Nephrology underlying Nephrology
required and urinalysis urinalysis and consultation disease consultation
every year renal function
testing every 6
months

100
4. ALGORITHM FOR MANAGEMENT OF SNAKE-BITE

Suspected snake-bite

. Neuroparalytic
Overt Bite Occult Bite symptoms with no local
History of bite nonvenomous No history of Krait signs
(70%)/venomous (30%) bite . Severe abdominal
pain, vomiting

Asymptomatic Dry bite Symptomatic

Predominant symptom manifestation . ASV
. Atropine and
neostigmine (Not to be
Anxiety, Palpitations, given in confirmed krait
Tachycardia,Paresthaesia
bite)
. Ventilation

Observe for 24
hours

Progressive painful Neuroparalytic Vasculotoxic Myotoxic

swelling

Viper Russel’s viper Sea snake

Cobra Krait
Saw Scale viper

. Local necrosis . Ptosis . Bleeding . Muscle ache

. Ecchymosis . Diplopia . Demonstrable . Muscle swelling
. Blistering . Dysarthria coagulopathy . Involuntary
. Painful . Dysphonia (20WBCT contractions of
swelling . Dyspnoea incoagulable) muscles
. Compartment . Dysphagia . Shock . Compartment
syndrome . Paralysis . Acute kidney injury syndrome.

ASV . ASV . ASV . ASV

. Atropine and . Supportive . Supportive
neostigmine (Not to treatment treatment
be given in . Dialysis . Dialysis
confirmed krait bite) . Blood transfusion
. Ventilation

101
 5. ALGORITHM FOR EVALUATION OF NEWLY IDENTIFIED CHRONIC KIDNEY DISEASE (CKD)

Newly identified CKD

Obtain ultrasound, urinalysis and microscopy, protein-creatinine ratio

Ultrasound shows obstruction?

Yes No

Relieve obstruction, if kidney function is determined to Is there albuminuria or RBC cast/

be salvageable by imaging or renal scan dysmorphic RBCs in urine?

Yes No

Evaluate for glomerulonephritis Evaluation depends on urinalysis

Sterile pyuria Normal urinalysis

Evaluate for interstitial nephritis High risk for renovascular disease?

No Yes

Follow serum creatinine. Evaluate for renovascular disease

Does creatinine remain
stable?

Yes No

Is there evidence of marked

chronicity on imaging?

Yes No

Kidney biopsy
No further evaluation. Follow closely for renal
replacement therapy.

102
 6. ALGORITHM FOR EVALUATION OF HYPONATREMIA

Hyponatremia

Serum osmolality
0
0 0

Normal Low High

(280 – 295 mosm/kg) (< 280 mosm/kg) (> 295 mosm/kg)

Isotonic (Pseudo) Hypotonic Hypertonic

hyponatremia hyponatremia hyponatremia
1. Hyperproteinemia 1. Hyperglycemia
2. Hyperlipidemia 2. Mannitol, Sorbitol,
Glycerol, Maltose
Volume status 3. Radiocontrast
agents
0
0 0

Hypovolemic Euvolemic Hypervolemic

0 0

1. SIADH Edematous
2. Post-op hyponatremia states
3. Hypothyroidism 1. Heart
0
4. Psychogenic polydypsia failure
5. Beer potomania 2. Cirrhosis of
6. Adrenocorticotropin liver
deficiency 3. Nephrotic
Syndrome
4. Advanced
UNa+< 10 mEq/L UNa+> 10 mEq/L renal failure
Extra-renal salt loss Renal salt loss
1. Dehydration 1. Diuretics
2. Diarrhoea 2. Nephropathies
3. Vomiting 3. Mineralocorticoid
deficiency
4. Cerebral salt wasting

103
7. ALGORITHM FOR EVALUATION OF ACUTE KIDNEY INJURY

Increase of serum creatinine ≥ 0.3 mg/dl in 48 hrs or increase by ≥ 1.5 times of baseline known or
presumed to have occurred within 7 days or urine volume < 0.5 ml/kg/hr for 6 hrs

Yes
Obtain ultrasound. Does it show obstruction? Address obstruction

No

Does history and examination Yes

Replete volume and recheck creatinine
suggest volume depletion?
No
No
Get urinalysis/microscopy Did Creatinine return to baseline?
and protein-creatinine ratio

Is there abnormal proteinuria Yes

Evaluate for glomerulonephritis
and/or haematuria?
No

Is there sterile pyuria? Yes Evaluate for acute interstitial nephritis

No

Does history/physical examination suggest sepsis, Yes

Evaluate for ATN
shock/hypotension, or nephrotoxin exposure?
No

Depending on history, examination and lab

If no apparent cause and creatinine
investigations, consider less common causes like
continuously rising or severely elevated,
rhabdomyolysis, tumour lysis syndrome, acute
then consider kidney biopsy
vascular obstruction, etc

If creatinine only mildly elevated and not rising,

then individualise further assessment as per
patient preference and risk benefit ratio (consider
nuclear studies)

104
8. ALGORITHM FOR EVALUATION OF POLYURIA

Exclude pseudohyperkalemia
Does the patient have one or more clinical manifestations of hyperkalemia?
These include 1. Cardiac conduction abnormalities or arrhythmias
2. Muscle weakness or paralysis
Polyuria
(Urine output > 3 L/d)

Urine Osmolality

Uosm< 100 mOsm/kg Uosm = 100-300 mOsm/kg Uosm> 300 mOsm/kg

(Water diuresis) (Mixed Polyuria) (Solute diuresis)

. Psychogenic polydipsia . Partial DI (Central & . Hyperglycemia

. DI (Central & nephrogenic) nephrogenic) . Azotemia
. Simultaneous water and . High solute intake
solute intake ü IV fluids
. CKD ü Enteral and
parenteral
nutrition
ü Exogenous
supplements

Water deprivation test 24 hour urine collection

(Estimation of osmoles)
. Urine sodium
. Urine potassium
. Urine glucose
. Urine urea nitrogen
. Other osmoles

105
 9. ALGORITHM FOR RISK STRATIFICATION AND MANAGEMENT OF HYPERKALEMIA

Exclude Pseudology

No
Yes
Serum potassium > 6.5 meq/L

Yes No

Are all three of the following present?

. Serum potassium > 5.5 meq/L
. Significant renal impairment
. Ongoing tissue destruction (rhabdomyolysis, tumour lysis syndrome, crush
injury) or ongoing potassium absorption (significant GI bleeding)

-
Yes No

Hyperkalemic emergency
Patient should be treated with rapidly acting therapies (e.g. IV calcium or Is serum
Glucose-Insulin infusion) in addition to therapies that remove potassium from potassium > 5.5
body (Haemodialysis, Gastrointestinal cation exchanger and/or diuretics) meq/L

-
-
Yes -
No
-
Does the patient have severe renal
impairment (ESRD or oliguria)?

-
-
Yes -
No -
-
Does the patient need to be optimised
- for an impending surgery?

-
0
Yes -
No
-
- -
Lower potassium promptly using therapies Potassium can be lowered slowly by
that remove potassium from body, use of diuretics or gastrointestinal
especially haemodialysis for ESRD patients. cation exchanger. Stop ACEI/ARBs,
Stop ACEI/ARBs, remove any external source remove any external source of
of potassium like fruits, juices etc. potassium like fruits, juices etc.

106
10. ALGORITHM FOR DIAGNOSIS OF HYPERCALCEMIA

Elevated serum calcium; correct for serum albumin, recheck ionised calcium

Measure intact PTH

Elevated
Upper normal range Low normal or low
Primary or minimally elevated
hyperparathyroidism Measure
Primary hyperparathyroidism . PTHrp
likely, consider Familial . 1, 25- dihydroxy Vit D
hypocalciuric hypercalcemia . 25- Hydroxy Vit D

If PTHrp elevated; humoral If 1, 25- dihydroxy Vit D elevated; If 25- Hydroxy

hypercalcemia of malignancy lymphoma, granulomatous Vit D elevated;
likely diseases (Sarcoidosis, Vitamin D
Tuberculosis) more likely intoxication
likely

If none, then measure

. SPEP
Multiple Myeloma Abnormal
. UPEP
. Serum free light chain assay

Normal

Assess for other causes like Vit A

Intoxication, Hyperthyroidism

107
BANGALORE
MEDICAL
CONGRESS