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

Oncology

Pulmonology

Rheumatology – Wg Cdr Harish Kumar

Haematology – Wg Cdr Harshit Khurana

Nephrology – Wg Cdr D Mahapatra, Wg Cdr VK Jha

– Col RK Anadure VSM, Wg Cdr Jitesh Goel – Gp Capt Kishore Kumar

– Wg Cdr Safia Ahmed

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

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

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.

Air Cmde DS Chadha

Consultant & HOD Mob: 9449050819

Contents Sl. Department Wise Algorithm

Page No

No.

1. Cardiology

2. Endocrinology

3. Gastroenterology

4. Neurology

5. Oncology

6. Pulmonology

7. Rheumatology

8. Haematology

9. Nephrology

Cardiology

1. APPROACH TO CHEST PAIN

Assess Vital Signs

Stable

Unstable

(Localised STE and low suspicion for dissection)

ST depression Yes and/or TWI

Diffuse STE+ PR depressions

Obtain 12-lead ECG and CXR

Stabilize. Assess for • STEMI

• Massive PE

• Aortic dissection

• Pericardial Tamponade

STEMI

Elevated and hx C/w ACS

Normal and hx c/w ACS

ECG diagnostic or suggestive

NSTEMI

Check cardiac markers or necrosis

↑area of lucency between lung parenchyma and chest wall

Pneumothorax

Dissection

No Dissection

Low

Aortic dissection

CXR diagnostic or suggestive

Yes

Widened mediastinum (and hx c/w AoD)

Infiltrate (and hx and labs c/w infections)

NSTEMI

Possible UA

Pericarditis

Dedicated imaging to access for AoD (CT, MRI, Echo)

Assess risk for ACS and check cardiac markers of necrosis

Assess risk for Pulmonary embolism

Assess risk for Aortic dissection

Hx c/w ACS and biomarkers elevated

Low

Neg

High

Neg

High +

Neg

Check D-dimer

Imaging (CT or V/Q)

Imaging (CT,MRI,TEE)

Hx c/w ACS and biomarkers normal

Hx not c/w ACS and biomarkers elevated

Hx not c/w ACS and biomarkersnormal

NSTEMI vs alternative cause of cardiac injury

Consider alternative diagnosis

Consider alternative diag8nosis

Possible UA

Consider alternative diagnosis

Pneumonia

Aortic dissection

2. PRE HOSPITAL MANAGEMENT OF STEMI

Activate

EMS: Emergency medical services

PCI: Percutaneous coronary intervention STEMI: ST- segment myocardial infarction

EMS

EMS triage

EMS on scene Encourage 12 Lead ECGs Consider prehospital fibrinolytic if capable and EMS-to-needle time<30 min

Hospital fibrinolysis Door-to-needle time<30 min

Patient symptom onset of

EMS dispatch

STEMI

Goals

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

Inter hospital transfer

EMS

Patient Dispatchon scene EMS transportEMS transport device<90 min

Not PCI capable

Hospital arrival STEMI confirmed 12- lead ECG (<10 min)

PCI capable

3. INITIAL REPERFUSION STRATEGIES FOR STEMI PATIENTS

Not PCI capable

If anticipated FMC-to-device time >120 min(class I)

Fibrinolysis

If anticipated FMC-device

<120 min (class I)

Rescue (class IIa)

Routine invasive (3-24 hrs) (class IIa)

Ischemia driven (class I)

Initially seen at PCI-capable hospital

(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

Clinical course/non invasive risk stratification

Late hospital care and secondary prevention

Transferred for PCI or CABG

PCI capable

Primary PCI

Table 1: Comparison of approved fibrinolytic agents

Agent

Dose

Fibrin specificity

Fibrinogen depletion

Antigenic

Patency rate

(90 min TIMI III flow)

Streptokinase

1.5 million units infusion over 30-60 min

Marked

Yes

60-68%

Tenecteplase(TNK)

Single IV weight based bolus*

++++

Minimal

85%

Reteplase(r-PA)

10 units + 10 units boluses 30 min apart

Moderate

84%

Alteplase(t-PA)

90 min weight based infusion#

Mild

73-84%

*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

Ant previous intracranial haemorrhage

Known structural cerebral vascular lesion

Known malignant intracranial neoplasm

Ischemic stroke within 3 months (except within 4.5 hours)

Suspected aortic dissection

Active bleeding or bleeding diathesis (excluding menstruation)

Significant closed head or facial trauma within 3 months

Intracranial or intra spinal surgery within 3 months

Uncontrolled hypertension unresponsive to emergency therapy

For streptokinase previous treatment with streptokinase within 6 months

4. IN HOSPITAL MANAGEMENT OF STEMI

Initially seen at a PCI- capable hospital

DIDO time< 30 min

Send to cathlab for primary PCI FMC- device time < 90 min (class I, level of evidence A)

Initially seen at a non PCI- capable hospital

Transfer for Primary PCI FMC- device time as soon as possible and < 120 min (class I: level of evidence :B)

Administer fibrinolytic

agent within 30 min of arrival when anticipated FMC device time > 120 min (class I:level of evidence :

Diagnostic angiogram

Medical therapy only

CABG

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

PCI

STEMI patient who is a candidate for reperfusion

Urgent transfer for PCI patients with evidence of failed reperfusion or reocclusion (classIIa; level of evidence: B)

Transfer for angiography and revascularisation within 3-24 hr for other patients as part of an invasive strategy (classIIa, level of evidence : B)

5. MANAGEMENT OF NSTE – ACS

NSTE-ACS Definite or likely

Ischemia-guided strategy

Initiate DAPT and Anticoagulant therapy

1. ASA(Class I; LOE:A)

2. P2Y 12 Inhibitor (in addition to ASA)

(Class I; DOE B) Clopidogrel or Ticagrelor

3. Anticoagulant

UFH(Class I; LOE:B) or Enoxaparin (Class I; LOE : A) Fondaparinux (Class I; LOE: B)

Initiate DAPT and Anticoagulant therapy

1. ASA(ClassI;LOE:A)

2. P2Y12Inhibitor(inadditiontoASA)

(Class I; DOE B) Clopidogrel or Ticagrelor

3. Anticoagulant

UFH(Class I; LOE:B) or Enoxaparin (Class I; LOE : A) or Fondaparinux (Class I; LOE: B) or Bivalirudin (Class I; LOE :B)

Can consider GPI in addition to ASA and P2Y12 inhibito in high risk(eg. Troponin positive) pts

(Class II b; LOE:B)

• Eptitibatide • Tirofiban

Medical therapy chosen based on catheter findings

Therapy effective

Therapy ineffective

PCI with stenting initiate/continue antiplatelet and anticoagulant therapy

1. ASA(ClassI;LOE:B)

2. P2Y12Inhibitor(inadditiontoASA)(Class

I;LOE B)

• Clopidogrel (Class I; LOE B) or

• Prasugrel (Class I; LOE B)or

• Ticagrelor(Class I; LOE B)

3. GPI(ifnottreatedwithbivalirudinatthe

time of PCI)

• High risk features not adequately

pretreated with clopidogrel(Class I; LOE B)

• High risk features adequately pretreated

with clopidogrel (Class IIa;LOE:B)

4. Anticoagulant

• Enoxaparin (Class I; LOE : A) or

• Bivalirudin (Class I; LOE: B)or

• Fondaparinux as the sole anticoagulant

(Class III; Harm LOE: B) or

• UFH(Class I; LOE:B) or

CABG initiate/continue ASA therapy and discontinue P2Y12and /or GPI therapy

1. ASA(ClassI;LOE:A)

2. DiscontinueClopidogrel/ticagrelor5days

before, and Prasugrel at least 7 days

before elective CABG

3. DiscontinueClopidogrel/Ticagrelorupto

24 hrs before urgent CABG (Class I: LOE;B) May perform urgent CABG < 5 days after clopidogrel/ Ticagrelor and < 7 days after Prasugrel discontinued.

4. Discontinueeptifibatide/Tirofibanatleast 2-4 hrs before and abciximab> 12 hours before CABG(Class I: LOE:B)

Late hospital/Post hospital care

1. ASAindefinitely(ClassI;LOE:A)

2. P2Y12Inhibitor(ClopidogrelorTicagrelor)

in addition to ASA up to 12 months of

medically treated (Class I:LOE:B)

3. P2Y12Inhibitor(ClopidogrelorTicagrelor)

in addition to ASA at least 12 months if treated with coronary stenting (Class I:LOE:B)

Early invasive strategy

6. MANAGEMENT OF ACUTE HEART FAILURE

Patient with acute heart failure(AHF)

Bedside assessment to identify haemodynamic profiles

YES

(95% of all AHF patients)

‘Wet ‘ Patients

Yes

(5% of all AHFpatients)

Presence of congestion?

ADEQUATE PERIPHERAL PERFUSION ?

‘Dry’ patients

Yes

= compendated

Yes

Hypovolemic

Dry & warm Adequately perfused

Dry & cold Hypoperfused

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

Adjust oral therapy

Consider fluid challenge, Consider inotropic agent if still hypoperfused

Vascular type fluid redistribution Hypertension predominates

‘Wet and warm’ patient (typically elevated or normal systolic blood pressure)

Cardiac type fluid accumulation Congestion pre dominates

‘Wet and cold’ patient

Systolic blood Pressure< 90mmHg

• Vasodilator • Diuretic

• Diuretic

• Vasodilator

• Ultra

filtration(Consider if diuretic resistance)

• Inotropic agent

• Consider vasopressor in

refractory cases

• Diuretic ( when perfusion

corrected)

• Consider mechanical

circulatory support if no response to drugs

• Vasodilators

• Diuretics

• Consider

inotropic agent in refractory cases

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:

• SVT and BBB

• Antidromic AVRT

Vagal manoeuvres or adenosine

Yes or unknown

Previous myocardial infarction or structural heart disease?If yes. VT

is likely

Atrial fibrillation

Atrial flutter/AT with variable conduction and

a) BBB or

b) Antegrade conduction

via AP

QRS morphology in precordial leads

V rate faster than A rate

A rate faster than V rate

Atrial tachycardia Atrial Flutter

RBBB pattern

• QR,RsorRr’inV1

• Frontal plane axis

• Range from +90 VT

degrees to -90 degrees

LBBB pattern

• R in V1 longer than 30 msec

• R to nadir of S in V1 VT greater than 60 msec

• qR or qS in V6

Typical RBBB SVT Or LBBB

1: 1 AV relationship ?

Precordial leads

• Concordant

• No R/S pattern VT

• Onset of R to nadir

longer than 100 msec

8. APPROACH TO NARROW QRS TACHYCARDIA

Yes

Visible P waves

Atrial rate greater than ventricular rate

Atrial flutter Atrial tachycardia

Narrow QRS tachycardia (QRS < 120 ms)

Regular

Atrial fibrillation

Atrial tachycardia /flutter with variable block

Yes

MAT

Analyse RP interval

Short (RP <PR)

RP > 70 ms

Long (RP>PR)

Atrial tachycardia PJRT

Atypical AVNRT

RP < 70 ms

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

9. MANAGEMENT OF VENTRICULAR FIBRILLATION/PULSELESS VT

VENTRICULAR FIBRILLATION OR PULSELESS VENTRICULAR TACHYCARDIA

Deliver single defibrillator shock Biphasic wave form 120-200J Monophasic wave form -360J

Resume CPR-check rhythm

Continue CPR and go algorithm for asystole

/PEA

Post resuscitation care

Continue CPR, 2 min then recheck rhythm

Deliver single defibrillator shock; if VF or VT persists, continue CPR, 2 min and give

epinephrine, 1 mg IV (repeat q3-5 times )

Pulse Restored

VF or VT Persists or recurs

VF or VT persists

VF or VT Persists or recurs

Asystole or PEA

Pulse Restored

Asystole or PEA

Deliver single defibrillator shock continue CPR

Post resuscitation care

Metabolic support as

indicated

Continue CPR

Continue CPR and go algorithm for asystole /PEA

Amiodarone [primary]: 300mg bolus then 150 mg Over 10 min, 1 mg/min Lidocaine

1.5 mg/kg: repeat in 3-5 min

Magnesium sulphate

1-2g IV [polymorphic VT]

Procainamide

30 mg/min, to 17 mg/kg [monomorphic VT]

Figure 9: ACLS for VF/Pulseless VT

Defibrillate [max recommended energy]: Drug-shock-Drug-Shock…

CPR: Cardio pulmonary resuscitation PEA: Pulseless electrical activity, VF: Ventricular fibrillation, VT: Ventricular tachycardia 17

10. MANAGEMENT OF BRADYARYTHMIA/ ASYSTOLE / PEA

Brady arrhythmia/ Asystole

ASASASAasyst

Confirm asystole

Pulse less electrical activity (PEA)

Assess pulse , blood flow

Maintain continuous CPR ole

[Intubate and establish IV access]

Indentify and treat reversible causes ,continue CPR

• Hypoxia

• Hyper/hypokalemia

• Severe acidosis

• Drug overdose

• Hypothermia

• Hypovolemia Pulmonary embolus

• Hypoxia Drug overdose

• Tamponade Hyperkalemia

• Pneumothorax Severe acidosis

• Hypothermia massive acute MI

•

• Hypoxia

• Ta

• Pneumothorax •H

Pulse and circulation Returned

Paced rhythm and pulse

Figure 10: ACLS for patients with bradyarrythmicasystolic arrest and PEA

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

Return of pulse and circulation mponade

Asystole or PEA persists (Continue CPR)

ypothemia

If VF or VT emerges, go

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)

Pacing: External or pacing wire

Post resuscitation care

11. APPROACH TO SYNCOPE

T- LOC suspected syncope

Syncope

Certain diagnosis

Treatment

High risk

Initial evaluation

Uncertain diagnosis

Risk stratification

Non syncopal T-LOC

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

T-LOC : Transient loss of consciousness

Low risk recurrent syncopes

Confirm with specific test or specialist consultation

Low risk single or rare

Early evaluation and treatment

Delayed treatment guided by ECG documentation

Cardiac or neutrally medicated tests as appropriate

No further evaluation

• May require lab investigations

• Risk for short term serious events

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 by alternative diagnosis

Treat as per guidelines for stable ischemic heart disease

Possible ACS, but non diagnostic ECG and normal troponin

Treat as per guidelines for ACS

Observe

Follow up at 1-3 hr, ECG & troponin

No recurrent pain Negative troponin and ECG

Elevated troponin or ischemic ECG changes

Very low clinical risk

Not very low clinical risk

Non invasive testing Positive

Negative

Discharge to home: Arrange for outpatient follow up

Figure 12: Algorithm for evaluation and management of patients suspected of having ACS 20

Endocrinology

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

ACTH test

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.

Bone age

Significantly increased

Normal

DHEAS and testosterone

Premature pubarche

DHEAS>115 mcg/dl or testosterone>20 ng/dl or bone age>120% height age

DHEAS 40-115 mcg/dl or

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

Premature adrenarche

17- hydroxyprogesterone and/or other steroid intermediate

Response elevated >10SD

Response normal or mildly elevated

Dexamethasone androgen supression test

Steroid pattern atypical

Dexamethasone androgen supression test

Supression normal

Supression subnormal

Congenital adrenal hyperplasia

Exaggerated adrenarche Steroid metabolism

disorders

Cushing syndrome Glucocorticoid resistance

Virilising tumour

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

Drug induced PAI

Measure serum 21 OH Abs

Antibodies positive

Males: Measure plasma VLCFA to rule out adrenoleukodystrophy(even in the absence of neurologic symptoms

Autoimmune adrenal insufficiency

Elevated VLCFA

Evidence of other autoimmune disorders

If yes polyglandular autoimmune syndrome

Antibodies negative

If yes adrenoleukodystrophy

Confirmatory molecular genetic testing required

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

If no adrenal CT scan

Abnormal

Normal

If not isolated autoimmune adrenal insufficiency

Possible etiologies: adrenal hemorrhage, infiltrative disease, malignant tumours metastasis, infections

Idiopathic PAI

3. DIAGNOSTIC APPROACH TO SUSPECTED ADRENAL INSUFFICIENCY

Basal plasma ACTH, cortisol 60 minutes ACTH 250 mcg test

Normal

Indeterminate cortisol results or suspected pituitary disease

Low cortisol Low ACTH

Low cortisol High ACTH

No adrenal insufficiency

Metyrapone or ITT

Secondary or tertiary adrenal insufficiency

Primary adrena linsufficiency

Absent or subnormal response

Normal cortisol response

CRH stimulation test

Adrenal insufficiency

No adrenal insufficiency

Exaggerated and prolonged ACTH response

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.

Absent or subnormal ACTH response

Tertiary adrenal insufficiency

Secondary adrenal insufficiency

4. DIAGNOSIS OF CUSHING’S SYNDROME

Cushing’s syndrome suspected

Perform one of the following test

Exclude exogenous glucocorticoid exposure

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 evaluation)

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

Abnormal

Normal (CS unlikely)

Cushing’s syndrome

5. TESTING TO ESTABLISH THE CAUSE OF CUSHING’S SYNDROME

Adrenal CT/MR imaging

ACTH independent Cushing’s syndrome as described

Measure ACTH

Supressed ACTH <5 pg/ml

Intermediate ACTH 5 to 20 pg/ml

CTH response

Normal to high ACTH >20 pg/ml

ACTH independent Cushing’s syndrome

CRH or desmopressin test

CRH stimulation AND dexamethasone supression test

Pituitary MRI

No ACTH response

Tumour>6 mm to undergo CRH stimulation or dexa supression test

Tumour < 6mm to undergo IPSS

ACTH dependent Cushing’s syndrome

IPSS

Adrenal tumour(s)/hyper plasia

Central step up (Cushing’s disease)

No central step up

Ectopic ACTH secretion

Adequate supression or stimulation

Mixed or negative 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.

6. ALGORITHM FOR THE DIAGNOSIS OF ACROMEGALY

If IGF1 normal acute acromegaly ruled out

IGF-1

If elevated OGTT with GH levels

GH supressed

Inadequate supression

Active acromegaly ruled out

Pituitary MRI

If normal Chest and abdominal CTand GHRH measurement

If mass or empty sella then GH secreting 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.

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- MIBG scan only if paraganglioma suspected or mass>10 cm

If negative abdominal iimaging reassess with functional imaging like 123i-MIBG or 68-Ga DOTATATE or FDG PET before concluding 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.

9. EVALUATION OF THYROID NODULE

Thyroid nodule on palpation or imaging

TSH normal or high

Solitary or multiple nodule

Apparent clinical nodule not demonstrated on imaging

< 1cm do clinical follow up

>1 cm

TSH supressed

Radionuclide thyroid scan to rule out hyperfunctioning nodule

Radioiodine ablation or surgery if hyperfunctioning nodule

Clinical follow up

US guided fine needle aspiration

If malignant or suspicious offer thyroid surgery

Benign

Unsatisfactory specimen

Follow up in 06 months

Repeat aspiration at 4 weeks to mirror two other endpoint

Gastroenterology

1. MANAGEMENT OF ACUTE ABDOMINAL PAIN Acute abdominal

Evaluation

Resuscitation Urgent surgical constitution

Consider FAST examination

Consider laparotomy

Appendix protocol CT

In female patients, consider pelvic US or CT

RUQ US

Upright abdominal film or oral contrast CT

Upright abdominal film or oral contrast

Pain “ABC”

Prostration; hemodynamically unstable

Perforated viscus

Diverticulitis No Mesenteric infarction

Acute pancreatitis

Yes

Nausea, vomiting, Yes obstipation, constipation,

abdominal distention; prior surgery

Sudden onset, diffuse Yes pain; involuntary guarding, rebound tenderness,

peritonitis

RLQ pain (gradual onset); RLQ tenderness, localized rebound tenderness

Gradual onset of RUQ cramping pain; history of postprandial discomfort

MANAGEMENT OF JAUNDICE

History, Physical examination, routine laboratory tests

Therapeutic intervention

Biliary Obstruction

Dilated

bile ducts ERCP or

THC

Yes

Biliary tract obstruction a consideration ?

Yes

Positive

Specific therapy

Alkaline Phosphates No

Evaluate for hemolysis, hereditary hyperbilirubinemia

Biochemical studies for specific causes of liver disease

or aminotransferases elevated ?

No biliary obstruction

Abdominal US or CT

Nondilated bile ducts

Negative

Consider liver biopsy

High

Dilated Bile ducts

Clinical likelihood of biliary obstruction

Low

Intermediate

Nondilated Consider bile ducts

MRCP or EUS

3. MANAGEMENT OF DYSPEPSIA

Uninvestigated dyspepsia

70%

Functional dyspepsia

Eradicate if possible for helicobacter pylori and not already treated

Empirical Therapy:

“Test and treat” PPI Consider prokinetic agent

No response

Endoscopy 30%

Organic dyspepsia

Peptic ulcer

Esophagitis Celiac disease Giardiasis Pancreatitis Biliary disease Others

Postprandial distress syndrome

Prokinetic agent Acotiamide 5-HT1A agonist

Acid suppressive therapy

Epigastric pain syndrome

Acid suppressive therapy

Prokinetic agent Acotiamide 5-HT1A agonist

Antidepressant,

if symptoms refractory

4. VOMITING

Chemotherapy, radiotherapy, or surgery?

Yes

Standard management with 5-HT3 antagonist, glucorticoids

Obtain relevant medical history, basic blood tests, and pregnancy test, if applicable

Suspicion of gastrointestinal or systemic infection?

Suspicion of drug or toxic-induced emesis?

Yes

Remove offending agent. If uncertain, perform toxicology screen or measure drug level. Central antiemetics

Neurologic or vestibular manifestations?

Electrolyte or glucose imbalance?

Correct metabolic derangements. Consider testing for adrenal insufficiency antiemetic agent, e.g., metoclopramide 0.1-1mg/kg/6 hr intravenously

Yes

MRI/CT of the brain, other neurologic and ENT Studies if necessary

Confirm by cultures, serological testing, imaging studies, as appropriate. Antiemetic agent, e.g., metoclopramide 0.1-1mg/kg/6 hr intravenously

No No

Investigate possible motility disorder, other less common causes

Gastrointestinal No Yes obstruction

suspected?

Yes

Abdominal CT, upper endoscopy, or UGI series

Mechanical obstruction Yes confirmed?

Motion sickness:

Antihistamine or muscarinic M1 blockers Other neurologic disorder: Central antiemetics

Specific treatment

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 Other possible diagnosis include painful gynecologic disorders (e.g., endometriosis)

Do appropriate diagnostic work-up

Yes

Is pain associated with bowel movements, eating, or menses?

Alarm features identified on history or physical examination?

Suspicion that pain is feigned?

No FAPS

Yes

Referral to mental health care professional to exclude malingering

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)

No source identified

Upper endoscopy or push enteroscopy

No source identified: RBC scintigraphy Angiography

No source indentified:

Consider repeat endoscopic studies, capsule endoscopy, balloon enteroscopy, or surgery

Source identified

Source identified: treat appropriately (see Figs.20-1 and 20-2)

Source identified: Arteriographic embolization or surgery

7. UPPER GI BLEED

Admission in Intensive care unit

Hematochezia, syncope, shock, comorbidities, onset of bleeding in hospital

Severe upper GI bleeding History and physical examination

Type and crossmatch, complete blood count, chemistry panel, liver biochemical test, coagulation tests, Transfusion as indicated

Hemodynamic resuscitation (ongoing)

Gastroenterology consultation

Stable vital signs and laboratory values; no active bleeding

Admission to standard hospital bed

Octreotide (bolus and infusion) if chronic liver disease suspected or confirmed

High dose PPI therapy if peptic ulcer suspected

Urgent upper endoscopy (after hemodynamic stabilization and intravenous prokinetic agent) within 6-12 hours of presentation

Hypotension, vomiting red blood, or hematochezia; place nasogastric tube

Stable vital signs with melena or coffee-ground emesis

Upper endoscopy (or push enteroscopy) within 24 hours of presentation

Specific endoscopic treatment

8. EXTRA-ESOPHAGEAL MANIFESTATION OF GERD

Possible extraesophageal

manifestation of GERD

Exclude underlying cardiac, thoracic, and head/neck disease

Test first strategy

24-hour pH study

Positive? Yes

Trial of twice daily PPI

Successful?

Yes

GERD maintenance therapy

Maximize medical therapy or consider antireflux surgery

Consider other diagnosis

Test first strategy

Trial of twice daily PPI

Successful? No

24-hour pH study

Positive?

Yes No

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

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.

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

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.

Neurology

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

YES NO

COAGULOPATHY

INCREASED ICP HEMODYNAMIC OR RESPIRATIRY INSTABILITY SKIN INFECTION OVER LUMBAR PUNCTURE SITE

START EMIRICAL ANTI-MICROBIAL THERAPY CONSIDER DEXAMETHASONE

CT HEAD NEGATIVE

YES

START EMIRICAL ANTI-MICROBIAL THERAPY CONSIDER DEXAMETHASONE

PERFORM LP

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

START EMIRICAL ANTI-MICROBIAL THERAPY CONSIDER DEXAMETHASONE

CONTRAINDICATIONS FOR LUMBAR PUNCTURE

YES

NO PERFORM LP

YES

2. EVALUATION OF PATIENT WITH INTERMITTENT WEAKNESS

VARIABLE WEAKNESS INCLUDES EOM, PTOSIS, BULBAR AND LIMB MUSCLES

EXAM NORMAL BETWEEN ATTACKS PROXIMAL>DISTAL WEAKNESS DURING ATTACK

EXAM USUALLY NORMAL BETWEEN ATTACKS PROXIMAL>DISTAL WEAKNESS DURING ATTACK

ACHR OR MUSK POSITIVE

ECG

ACQUIRED SEROPOSITIVE MG

DECREMENT ON 2-3 HZ RNS OR INCREASED JITTER ON SFEMG

CHECK FOR DYSMORHIC FEATURES GENETIC TESTING FOR ANDERSON- TAWII SYNDROME

MYOTONIA ON EXAMINATION

REDUCED LACTIC ACID RISE, CONSIDER GLYCOLYTIC DEFECT

NORMAL LACTIC ACID RISE CONSIDER CPT DEFICIENCY OR FA METABOLISM DISORDERS

CHEST CT FOR THYMO MA

YES

LAMBERT-EATON MYASTHENIC SYNDROME

CONSIDER : SERONEGATIVE MG, CONGENITAL MG, PSYCHOSOMATIC WEAKNESS

LOW POTASSIUM LEVELS

NORMAL OR ELEVATED POTASSIUM LEVELS

MUSCLE BIOPSY DEFINES SPECIFIC DEFECT

CHECK: VOLTAGE GATED CC ANTIBODIES, CHEST CT FOR CA LUNG

HYPOKALEMIC PP

HYPERKALEMIC PP, PARAMYOTONIA CONGENITA

YES

INTERMITTENT WEAKNESS MYOGLOBINURIA

YES

ABNORMAL

NORMAL

FOREARM EXERCISE

3. EVALUATION OF PATIENT WITH MYASTHENIA GRAVIS

OCULAR ONLY

GENERALIZED

CRISIS

MRI BRAIN

IF POSITIVE, REASSESS

ACTEYLCHOLINE ESTERASE-I (PYRIDOSTIGMINE)

PLASMAPHERESIS, INTRAVENOUS IG

IF UNSATISFACTORY

GOOD RISK(GOOD FVC)

POOR RISK (LOW FVC)

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.

EVALUATE FOR THYMECTOMY(THYMOMA, GENERLAISED MG, EVALUATE SURGICAL RISK, FVC)

INTENSIVE CARE (RESPIRATORY INFECTIONS, FLUIDS)

THYMECTOMY

THEN

EVALUATE CLINICAL STATUS; IF INDICATED, IMMUNOSUPPRESSION

IMPROVED

IF NOT IMPROVED IMMUNOSUPPRESSION

4. OP POISONING

CHECK AIRWAY, BREATHING, AND CIRCULATION.

SEVERITY

SYMPTOMS

SIGNS

ASSESS SEVERITY OF OP POISONING

RHINORRHEA, SWEATING, SALIVATION, NAUSEA, WEAKNESS, COUGHING, LACRIMATION, MILD BRADYCARDIA

PLACE PATIENT IN THE LEFT LATERAL POSITION, PREFERABLY WITH HEAD LOWER THAN THE FEET, TO REDUCE RISK OF ASPIRATION OF STOMACH CONTENTS.

INTUBATE THE PATIENT IF THEIR AIRWAY OR BREATHING IS COMPROMISED

RESTLESSNESS, CONFUSION, DYSPNEA, DISORIENTATION, ABDOMINAL PAIN, VOMITING, DIARRHEA, DROWSINESS

AND HYPOTENSION

PALLOR, MIOSIS/MYDRIASIS, BRADYCARDIA/

TACHYCARDIA, HYPOTENSION/ HYPERTENSION,

MUSCLE TWITCHING, FASCICULATION, RESPIRATORY DEPRESSION, BRONCHORRHEA, BRONCHOSPASM,

LOSS OF CONSCIOUSNESS CONVULSIONS, RESPIRATORY FAILURE, PULMONARY EDEMA, FLACCID PARALYSIS, INVOLUNTARY MICTURATION/DEFECATION CYANOSIS, DEEP COMA

AFTER STABILISATION AND ENSURING ADEQUATE AIRWAY,

MODERATE

GASTRIC DECONTAMINATION

• GASTRIC LAVAGE

• ACTIVATED CHARCOAL 25 G 2 HOURLY

REMOVAL FROM SURFACE OF SKIN, EYES AND HAIR

OBTAIN INTRAVENOUS ACCESS AND GIVE 1–3 MG OF ATROPINE AS A BOLUS, DEPENDING 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

AFTER ATROPINIZATION OCCURS, 10–20% OF ATROPINE

REQUIRED FOR ATROPINIZATION TO BE ADMINISTERED EVERY HOUR BY IV INFUSION.

NECK FLEXOR WEAKNESS INDICATES IMPENDING PERIPHERAL RESPIRATORY FAILURE (INTERMEDIATE SYNDROME).

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 G/H (OR OBIDOXIME 30 MG/HR) IN 0·9% NORMAL SALINE

TREAT AGITATION BY REVIEWING THE DOSE OF ATROPINE BEING GIVEN AND PROVIDE ADEQUATE SEDATION WITH BENZODIAZEPINES

CONTINUE THE OXIME INFUSION UNTIL ATROPINE HAS NOT BEEN NEEDED FOR 12–24 H AND THE PATIENT HAS BEEN EXTUBATED

MILD

DIZZINESS, ANXIETY, HEADACHE, TIGHTNESS OF BREATH

SEVERE

MONITOR FREQUENTLY FOR RECURRING CHOLINERGIC CRISES DUE TO RELEASE OF FAT SOLUBLE ORGANOPHOSPHORUS FROM FAT STORES.

5. EVALUATION OF SOLITARY SEIZURE

HISTORY OF EPILEPSY, CURRENTLY TREATED WITH ANTI-EPILEPTIC DRUGS

NO HISTORY OF EPILEPSY

ASSESS ADEQUACY OF ANTI-EPILEPTIC THERAPY, SIDE EFFECTS, SERUM LEVELS

LABORATORY STUDIES

CBC

ELECTROLYTES, CALCIUM, MAGNESIUM

SERUM GLUCOSE

LIVER FUNCTION TESTS, RENAL FUNCTION TESTS URINALYSIS

TOXICOLOGY SCREEN

NORMAL

ABNORMAL OR CHANGE IN NEUROLOGIC EXAM

LABORATORY STUDIES

CBC

ELECTROLYTES, CALCIUM, MAGNESIUM

SERUM GLUCOSE

LIVER FUNCTION TESTS, RENAL FUNCTION TESTS URINALYSIS

TOXICOLOGY SCREEN

POSITIVE METABOLIC SCREEN OR SYMPTOMS/SIGNS SUGGESTING A METABOLIC OR INFECTIOUS DISORDER

NEGATIVE METABOLIC SCREEN

SUBTHERAPEUTIC ANTIEPILEPTIC DRUG LEVELS

THERAPEUTIC ANTIEPILEPTIC DRUG LEVELS

FURTHER WORKUP LUMBAR PUNCTURE CULTURES ENDOCRINE STUDIES CT

FOCAL FEATURES OF SEIZURES

FOCAL ABNORMALITIES ON CLINICAL OR LAB EXAMINATION

OTHER EVIDENCE OF NEUROLOGIC DYSFUNCTION

APPROPRIATE INCREASE OR RESUMPTION OF DOSE

INCREASE AED DOSE TO MAXIMUM TOLERATED DOSES CONSIDER ALTERNATIVE AED DRUGS

TREAT UNDERLYING METABOLIC ABNORMALITIES

YES

TREAT IDENTIFIABLE METABOLIC ABNORMALITIES

ASSESS CAUSE OF NEUROLOGIC CHANGE

CONSIDER ANTIEPILEPTIC THERAPY

ADULT PATIENT WITH A SEIZURE

HISTORY

PHYSICAL EXAMINATION

EXCLUDE

SYNCOPE

TIA

MIGRAINE

ACUTE PSYCHOSIS

OTHER CAUSES OF EPISODIC CEREBRAL DYSFUNCTION

MRI IF FOCAL FEATURES PRESENT

TREAT UNDERLYING DISORDER

MRI AND EEG

CONSIDER: MASS LESION; STROKE; CNS INFECTION; TRAUMA; DEGENERATIVE DISEASE

CONSIDER ANTIEPILEPTIC THERAPY

IDIOPATHIC SEIZURES

6. MANAGEMENT OF STATUS EPILEPTICUS

IMPENDING AND EARLY SE (5 – 30 MINUTES)

ESTABLISHED AND EARLY REFRACTORY SE

(30 MINS – 48 HOURS)

GENERALISED CONVULSIVE OR “SUBTLE” SE

FOCAL COMPLEX, MYOCLONIC OR ABSENCE SE

LATE REFRACTORY SE (>48 HOURS)

THP(PTB)

5 MG/KG – 1-5 MG/KG/HR

OTHER MEDICATIONS LIDOCAINE, MAGNESIUM, VERAPAMIL, IMMUNOMODULATION

OTHER ANAESTHETICS ISOFLURANE, DESFLURANE, KETAMINE

OTHER approaches SURGERY, VNS, TMS, HYPOTHERMIA

IV MDZ 0.2 MG/KG – 0.2-0.6 MG/KG/HR IV PRO 2 MG/KG – 2-10MG/KG/HR

FURTHER IV/PO ANTIEPILEPTIC DRUG VPA, LEV, LCM, TPM, PGB, OR OTHER

IV BENZODIAZEPINE

LZP 0.1 MG/KG, OR MDZ 0.2 MG/KG OR CLZ 0.015 MG/KG

IV ANTIEPILEPTIC DRUG PHT 20 MG/KG OR VPA 20-30 MG/KG OR LEV 20-30 MG/KG

MONONEUROPATHY EDX

POLYNEUROPATHY EDX

EVALUATION OF OTHER DISORDER ORREASSURANCE AND FOLLOW-UP

IS THE LESION AXONAL OR DEMYELINATING? IS ENTRAPMENT OR COMPRESSION PRESENT?

AXONAL

DEMYELINATING WITH FOCAL CONDUCTION BLOCK

AXONAL

DEMYELINATING

IS A CONTRIBUTING SYSTEMIC DISORDER PRESENT?

CONSIDER VASCULITIS OR OTHER MULTIFOCAL DISORDERS

MULTIFOCAL FORMS OF CIDP

SUBACUTE COURSE

CHRONIC COURSE

UNIFORM SLOWING, CHRONIC

NONUNIFORM SLOWING, CONDUCTION BLOCK

7. EVALUATION OF PATIENT WITH NEUROPATHY

PATIENT COMPLAINT – ? NEUROPATHY

DECISION ON NEED FOR SURGERY (NERVE REPAIR, TRANSPOSITION, OR RELEASE PROCEDURE)

POSSIBLE NERVE BIOPSY

TEST FOR PARAPROTEIN, HIV,LYME DISEASE

REVIEW HISTORY FOR TOXINS, TESTS FOR ASSOCIATED SYSTEMIC DISEASE OR INTOXICATION

TEST FOR PARAPROTEIN, IF NEGATIVE

IF CHRONIC OR SUBACUTE: CIDP

IF ACUTE : GBS

TREATMENT APPROPRIATE FOR SPECIFIC DIAGNOSIS

IF TESTS ARE NEGATIVE, CONSIDER TREATMENT FOR CIDP

TREATMENT APPROPRIATE FOR SPECIFIC DIAGNOSIS

REVIEW FAMILY HISTORY : EXAMINE FAMILY MEMBERS, GENETIC TESTING

TREATMENT FOR CIDP

IVIG OR PLASMA EXCHANGE, SUPPORTIVE CARE

YES MONONEUROPATHY MULTIPLEX

EDX

HISTORY AND EXAMINATION COMPATIBLE WITH NEUROPATHY

GENETIC COUNSELLING IF APPROPRIATE

METHYLPRED/ PREDNISOLONE

REPEAT CLINICAL EXAM AND MRI IN 6 MONTHS

8. MANAGEMENT OF PATIENT WITH RRMS

ACUTE NEUROLOGIC CHANGE

STABLE

EXACERBATION

PSEUDOEXACERBATION

LOW ATTACK FREQUENCY OR SINGLE ATTACK NORMAL NEUROLOGIC EXAM LOW DISEASE BURDEN BY MRI

FUNCTIONAL IMAPAIRMENT

NO FUNCTIONAL IMAPIRMENT

IDENTIFY AND TREAT ANY UNDERLYING INFECTION OR TRAUMA

MILD

MODERATE OR SEVERE

SYMPTOMATIC THERAPY

NO INITIAL COURSE

YES

RELAPSING-REMITTING MS

OPTIONS:

1.INJECTABLES(GA OR IFN-BETA) 2.ORAL(DMF, FINGLOIMOD, TERIFLUONAMIDE) 3.NATALIZUMAB(IF JC VIRUS

OPTIONS:

1.ORAL(DMF, FINGOLIMOD

NEGATIVE)

GOOD RESPONSE

POOR RESPONSE OR INTOLERANT

CLINICAL OR MRI CHANGE

NO CHANGE

CONTINUE THERAPY

SUCCESSIVE T5R5IALS OF ALTERNATIVES

CONTINUE PERIODIC CLINICAL/MRI ASSESSMENTS

TERIFLUNOMIDE) 2.NATALIZUMAB(JC V NEG)

9. EVALUATION OF PATIENT WITH PERSISTENT WEAKNESS PERSISTENT MUSCLE WEAKNESS

Proximal > distal

Facial and scapular winging (FSHD)

Dropped head

Facial, distal, quadriceps; handgrip myotonia Myotonic muscular dystrophy

Proximal & distal (hand grip), & quadriceps

IBM

Distal

Distal myopathy

PM; DM; muscular dystrophies; mitochondrial and metabolic myopathies; toxic, endocrine myopathies

Ptosis, EOMs

MG; PM; ALS; hyperparathyroidism

OPMD; mitochondrial myopathy; myotubular myopathy

PATTERNS OF WEAKNESS ON NEUROLOGIC EXAMINATION

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

Oncology

1. TREATMENT OF PATIENTS WITH CARCINOMA OF UNKNOWN PRIMARY

Clinical presentation

Initial clinical, pathological evaluation

No primary site found

Specific treatable Subgroup

Anatomic primary site located

Additional testing if necessary for the specific cancer type (may include molecular testing of biopsy, tumor makers)

Consider comprehensive molecular profiling of tumor

Additional focused clinical, IHC studies based on initial results

No treatable

sub group identified

pecific treatment for subgroup

Gene expression assay of tumor

Tissue of Origin predicted

No tissue of Origin predicted

Site-specific treatment

Consider comprehensive molecular profiling of tumor

Empiric chemotherapy or clinical trial

Site-specific therapy or clinical trial

2. ALGORITHMIC APPROACH TO RISK ASSESSMENT OF TUMOR LYSIS SYNDROME

mall tumor urden

One abnormal test result

Two or more abnormal test result

Medium tumor burden

Laboratory TLS plus

one or more: Serum (Laboratory TLS)

creatinine >1.5 ULN, cardiac arrythmia,

seizure

Estimate tumor burden and lysis risk

S b

Low riskHigh risk

for lysisfor lysis uncertain for lysis

risk for lysis

Patient condition?

Uncertain

for lysis

Medium risk

Low risk

risk for lysis

High risk

Abnormalities:

• Renal dysfunction • Dehydration

• Low blood pressure • Acidosis

No abnormalities

Clinical TLS

inimal risk

High risk

Intermediate risk

Low risk

Intermediate risk

High risk

ophylaxis icated

Prophylaxis:

• Hydration

• Rasburicase

• Cardiac

monitoring

• Lab test every 6 to 8 hours

Prophylaxis:

• Hydration

• Allopurinol

rasburicase

• Lab test

every 6 to 8 hours

Prophylaxis:

• Hydration with or

without

allopurinol

• Close monitoring

Prophylaxis:

• Hydration

• Allopurinol

rasburicase

• Lab test

every 8 to 12 hours

Prophylaxis

• Hydration

• Rasburicas

• Cardiac

monitoring

• Lab tests

every 6 – 8 years

Prophylaxis

• Hydratio

• Rasburica

• Lab test every 4-6 hrs

No pr ind

: n

TLS: tumor lysis syndrome; ULN: upper limit of normal; ICU: intensive care unit

Laboratory tests (serum potassium, phosphorus, calcium, creatinine, uric acid)

Large tumor burden

3. SUGGESTED ALGORITHM FOR THE MANAGEMENT OF EPIDURAL SPINAL CORD COMPRESSION (ESCC)

Stable

Radiosensitivity of primary tumor

Unstable

Retropulsion of bone fragments into spinal cord?

Yes

Resistance or previously radiated

Vertebral bone metastasis with epidural extension

Access spinal stability*

Sensitive

cEBRT

High-grade ESCC?

Surgical decompression and fixation

High-grade ESCC?

Yes

Sensitive

Radiosensitivity of primary tumor

Spine stabilization

Resistance or previously radiated

SBRT

Surgical decompression and fixation followed by SBRT

Spine stabilization followed by eCBRT

Radiosensitivity of primary tumor

Resistance or previously radiated

SBRT

Sensitive

cEBRT

Triage

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

• 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

15I

Yes

Goal-directed therapy

Sepsis syndrome

30I

•

N o

• Resuscitation facilities

• Optimize hemodynamics & O2 delivery

• Initiate empiric antibacterial therapy

• Critical care service

Medical assessment

(within 15 min of triage)

Severe sepsis syndrome

(SIRS + altered mental status or hypoperfusion or hypoxia)

Identify potential sources of infection (LRT, URT, periodontium, skin, GI tract, GU tract)

eutropenic fever syndrome due to probable or documented infection together with systemic manifestation f infection)

Yes

• Supplemental O2

• Empirical antibacterial therapy

• IV 0.9 percent saline 1 L over 1 to

2 hours

60I

High

Low

Risk for medical complications

• Consider IV → PO or PO therapy

• Consider inpatient→ outpatient

• Discharge when physiologically are

controlled

• Duration 3 to 5 afebrile days (total to

10 days)

• Admission

• IV antibacterial therapy

• Discharge when physiologically

stable, comorbidities are controlled

• Duration 4 to 5 afebrile days (total

7 to 14 days)

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

2 yrly> 30 (if 3 reports Normal)

Within 3 yrs of sexual activity

70 yrs

Colon

FOBT Colonoscopy (? On request)

Yearly once in 10 years

50 yrs of age

Lifelong

Prostate

PSA

Not recommended

? On request

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

• Fosaprepitant

125 mg oral 150 mg IV

80 mg oral daily; 2 and 3

5-HT3 antagonist(one of the following

• Granisetron

• Ondansetron

• Palonosetron

2 mg oral; 1 mg or 0.01 mg/kg IV; 10 mg SQ

8 mg oral twice daily; 8 mg or 0.15 mg/kg IV

0.5 mg oral; 0.25 mg IV

Glucocorticoid

• Dexamethasone

• Ozanzapine

12 mg oral or IV (20 mg orally if using rolapitant)

5 to 10 mg

8 mg oral or IV daily; days 2 to 4 5 to 10 mg daily; days 2 to 4

Moderate emetic risk (30 to 90%) Non-carboplatin

Carboplatin based

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

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)

Low emetic risk (10 to 30%)

Glucocorticoid

• Dexamethasone

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)

4 to 8 mg oral or IV

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.

7. WORLD HEALTH ORGANIZATION (WHO) ANALGESIC LADDER

P A I N

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

+ adjuvant

Moderate to severe pain

Opioid (Codeine, Tramadol, etc.) + non-opioid,

+ adjuvant

Mild to moderate pain

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

+ adjuvant

Mild pain

Pulmonology

1. THEREFINEDABCDASSESSMENTTOOLFORCOPD

SPIROMETRICALLY CONFIRMED DIAGNOSIS

ASSESSMENT OF AIRFLOW LIMITATION

ASSESSMENT OF SYMPTOMS / RISK OF EXACERBATIONS

POST – BRONCHODILAT OR FEV1 / FVC < 0.7

FEV1 ( % PREDICTED)

GOLD 1 ≥80 GOLD 2 50-79 GOLD 3 30-49 GOLD 4 <30

0 OR 1 (NOT LEADING TO HOSPITAL ADMISSION

EXACERBATION HISTORY

≥ 2 OR ≥ 1 LEADING TO HOSPITAL ADMISSION

mMMRC0-1CAT<10 mMMRC≥2CAT≥10 SYMPTOMS

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

IDENTIFIABLE CAUSES FOR ILD?

HRCT

SURGICAL LUNG BIOPSY

YES

POSSIBLE UIP * INCONSISTENT W/UP *

NOT UIP +

UIP + PROBABLE UIP+/ POSSIBLE UIP + NON CLASSIFIABLE FIBROSIS +

MDD

IPF

NOT IPF

IPF/ NOT IPF PER TABLE 6

*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.

3. MANAGEMENT OF ASTHMA EXACERBATIONS IN PRIMARY CARE

PRIMARY CARE

MILD OR MODERATE

TALKS IN PHRASES ,PREFERS SITTING TO LYINGNOT AGITATED RESPIRATORY RATE INCRESED ACCESOPRY MUSCLES NOT USED PULSE RATE 100-120 BPM OXYGEN SATURATION (ON AIR) 90-95 % PEF> 50 % PREDICTED OR BEST.

START TREATMENT

SABA 4-10 PUFFS BY PMDI + SPACER REPEAT EVERY 20 MINUTES FOR 1 HOUR PREDNISOLONE :ADULTS 1MG/KG.MAX50 MG CHILDREN 1-2 MG/KG MAX 40 MG.

CONTROLLED OXYGEN (IF AVAILABLE) TARGETSATUIRATION 93-95 % (CHILDREN 94-98 %)

IMPROVIN

PATIENT PRESENTS WITH ACUTE OR SUB ACUTE ASTHMA EXACERBATION

ASSESS THE PATIENT

IS IT ASTHMA ?

RISK FACTORS FOR ASTHMA – RELATED DEATH ?

SEVERITY OF EXACERBATION .

SEVERE

TALKS IN WORDS , SITS HUNCHED FORWARDS , AGITATED RESPIRATORY RATE> 30 –PM ACCESSORY MUSCLE IN USE PULSE RATE> 120 BPM , OXYGEN SATURATION (ON AIR) <90% PES ≤ 50 % PREDICTED OR BEST .

LIFE THREATENING

DROWSY, CONFUSED OR SILENT CHEST .

URGENT

TRANSFER TO ACUTE CARE FACILITY

WHILE WAITING :GIVE SABA , O2,SYSTEMIC CORTICOSTEROID.

WORSENING

CONTINUE TRAETMENT WITH SABA AS NEEDED ASSESS RESPONSE AT ONE HOUR (OR EARLIER)

G ASSESS FOR DISCHARGE

SYMPTOMS IMPROVE NOT NEEDING SABA. PEF IMPROVING AND < 60-80 % OF PERSONAL BEST OR PREDICTED.

O2 SATURATION <94 %ROOM AIR RESOURCES AT HOME ADEQUATE.

ARRANGE AT DISCHARGE

RELIVER : AS NEEDED RATHER THAN ROUTINELY . CONTROLLER : START (BOX 3-4) ,OR STEP UP (BOX (4-2) CHECK INHALER TECHNIQUE ADHERANCE. PREDNISOLONE : CONTINUE ,USEUALLY FOR 5-7 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?

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

CULTURES +

YES

CULTURES –

CULTURES +

SEARCH FOR OTHER PATHOGENS, COMPLICATIONS ,OTHER DIAGNOSIS OR OTHER SITES OF INFECTION

ADJUST ANTIBIOTIC THERAPY,SEARCH FOR OTHER PATHOGENS, COMPLICATIONS,OTHE R DIAGNOSIS OR OTHER SITES OF INFECTION

CULTURES –

CONSIDER STOPPING ANTIBIOTICS

DE-ESCALATE ANTIBIOTICS,IF POSSIBLE.TREAT SELECTED PATIENTS FOR 7-8 DAYS & REASSESS

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

KNOWN OR SUSPECTED MPE

SYMPTOMATIC

IMPROVEMENT IN DYSPNEA

ASYMPTOMATIC

YES

LUNG RE-EXPANSION

YES

DISCUSSION OF RELATIVE RISKS/BENEFITS OF IPC vs PLEURODESIS vs COMBINATION APPROACHES

PLEURAL INTERVENTION NOT NEEDED (UNLESS FOR DIAGNOSTIC PURPOSES

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

INVESTIGATE FOR OTHER CAUSES OF DYSPNEA

LUNG RE- EXPANSION

PREDICTED VERY SHORT SURVIVAL**

TALC POUDRAGE OR TALC SLURRY +/- IPC

consider placement of IPC(indwelling pleural catheter)should also be considered in patients with failed pleurodesis or symptomatic loculated effusion)

PALLIATE DYSPNEA WITH : REPEAT THORACENTESIS IF NEEDED , OXYGEN,

EVIDENCE OF IPC – RELATED INFECTION

MORPHINE

YES

INITIATION OF ORAL ANTIBIOTICS BASED ON LOCAL SENSITIVES. ATTEMPT TO KEEP CATHETER

74 CONSIDER DAILY DRAINAGE AND /OR TALC SLURRY

IN PLACE (IPC)

CONSIDER DRAINAGE AS GUIDED BY SYMPTOMS OR LOCAL PROTOCOL

6. MASSIVE HAEMOPTYSIS

UNSTABLE PATIENT

INCUBATION TRANSFUSION THORACIC SURGERY CONSULT EARLY BRONCOSCOPY

MASSIVE HAEMOPTYSIS

INVESTIGATIONS FBC,U&ES,COAG,ABG,CXR,GR OUP AND CROSS MATCH

ADMIT TO HDU/ITU RESPIRATORY CONSULT

RESUSCITATION, OXYGEN SUPPLEMENTATION, CORRECT ANY COAGULOPATHY, CONSIDER TRANEXAMIC ACID

SUSPECTED PULMONARY EMBOLUS

STABLE PATIENT

CT THORAX

SPINAL CT ANGIOGRAM

BLEEDING SITE NOT LOCALISED

BRONCOSCOPY

BLEEDING SITE LOCALISED

INVESTIGATION FOR INTERSTITIAL LUNG DISEASE GOODPASTURES, VASCULITIS

INTERSTITIAL RETICULAR PATTERN

ENDOBRANCHIAL TAMPONADE

ANGIOGRAPHY

BLEEDING SITE LOCALISED

INFILTRATE

CAVITY

LESION

BLEEDING SITE NOT LOCALISED

CONSERVATIVE MANAGEMENT

SPUTUM CULTURE , AFB FUNGAL CULTURE

TB, ASPERGILLOMA ,ABSCESS

APPROPRIATE ANTIBIOTCS

BRONCHIAL ARTERY EMBOLISATION OR SURGERY

NODULE OR CYSTIC

BRONCOSCOPY ,INSTILLATION OF

PERSISTENT BLEEDING

IF INDICATED

ANTIFUNGAL AGENTS ,AS INDICATED

7. ALGORITHM FOR ANALYSIS OF PLEURAL FLUID BASED ON APPEARANCE

APPEARANCE OF PLEURAL FLUID

YES

HCT < 1%

BLOODY?

OBTAIN HEMOCRIT

HCT > 1%

HCT > 20%

YES

HEMOTHORAX

CLOUDY

YES

CLEAR

LIKELY DIAGNOSIS TUMOR,PULMONARY EMBLOUS,OR TRAUMA

BLOODINESS NOT SIGNIFICANT

GO TO CHEMICAL ANALYSIS

LOOK AT SUPERNATANT

CLOUDY

EXAMINE SEDIMENT

CHYLOTHORAX OR PSEUDOCHYLOTHORAX

CONSIDER

INSERTING CHEST TUBE

CHOLESTEROL CRYSTALS

YES

PSEUDOCHYLOTHORAX

<50 MG/ DL

PLEURAL FLUID TRIGLYCERIDES

50-110 MG/DL

>110 MG/DL

LIPOPROTEIN ANALYSIS

CHYLOMICRONS

CHYLOTHORAX

8. APPROACH TO A PATIENT WITH SUSPECTED PLEURAL EFFUSION

PATIENT WITH ABNORMAL CHEST RADIOGRAPH

SUSPECT PLUERAL DISEASE

LATERAL DECUBITUS CHEST RADIOGRAPHS, CHEST OR

ULTRASOUND

FLUID THICKNESS > 10MM

BLUNTING OF COSTROPHRENIC ANGLE?

YES

OBSERVE

ANY OF THE FOLLOWING MET? PF/SERUM PROTIEN > 0.5 PF/SERUM LDH >0.6, PF LDH >2/3 UPPER NORMAL SERUM LIMIT.

YES

TRANSUDATE

YES

EXUDATE

YES

PROBABLE EXUDATE

PATIENT HAS CHF OR CIRRHOSIS?

PLEURAL EFFUSION UNLIKELY

DIAGNOSTIC THORACENTESIS

TREAT CHF,CIRRHOSIS, OR NEPHROSIS

SERUM-PLEURAL FLUID PROTEIN GRADIENT >3.1

APPEARANCE OF FLUID GLUCOSE OF PLEURAL FLUID CYTOLOGY AND DIFFERENTIAL CELL COUNT OF PLEURAL FLUID .PLEURAL FLUID MARKER FOR TB.

N7T7-PRO BNP >1500

YES TREAT CHF

9. STEPWISE APPROACH TO ASTHMA TREATMENT

REVIEW RESPONSE

ASSESS

DIAGNOSIS.

SYMPTOM CONTROL &RISK FACTORS (INCLUDING LUNG FUNCTION). INHALER TECHNIQUE & ADHERANCE PATIENT PREFERENCE, ASTHMA MEDICATIONS, NON –PHARMOCOLOGICAL STRATERGIES, TREAT MODIFIABLE RISK FACTORS .

SYMPTOMS EXACERBATIONS SIDE EFFECTS PATIENT SATISFACTION LUNG FUNCTION.

PREFERREDC ONTROLLER CHOICE

O C O

RELIEVER

R T

ADJUST TREATMENT

STEP 3

LOW DOSE ICS/LABA**

STEP 4

MED/HIGH ICS/LABA

STEP 5

REFER FOR ADD ON

TREATMENT .Eg. TIOTROPIUM ANTI

IGE, ANTI-IL5

STEP 1

STEP 2 LOW DOSE ICS

CONSIDER LOW LEUKOTRIENE RECEPTOR DOSE ICS ANTAGONIST (LTRA) DOSE THEOPHYLLINE

MED HIGH ADD ADD LOW DOSE LOW DOSE ICS LOW TRIOTROPIUM+ OCS

DOSE ICS +LRTA MED /HIGH

(OR + THEOPH) DOSEICS +LRTA (OR + THEOPH)

THER ONTROLLER PTIONS

AS NEEDED SHORT –ACTING BETA2-AGONIST (SABA)

AS NEEDED SABA ORLOW DOSE ICS/FORMOTEROL

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

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.

CONSIDER STEPPING DOWN IF SYMPTOMS CONTROLL FOT 3 MONTHS + LOW RISK FOR EXACERBATIONS .STOPPING ICS IS NOT ADVISED.

EMEMBR O

PLHIV

PRESUMPTIVE TB PATIENT ( any 1 of the following- COUGH >2 WEEKS,FEVER >2 WEEKS, HAEMOPTYSIS, CXR ABNORMALITY

10. DIAGNOSTIC ALGORITHM FOR PULMONARY TB

SMEAR POSSITIVE AND CXR SUGGESTIVE OF TB

SMEAR POSITIVE ,BUT CXR NOT SUGGESTIVE OF TB

SMEAR NEGATIVE BUT CXR SUGGESTIVE OF TB

SMEAR NEGATIVE OR NOT AVAILABLE & CXR NOT SUGGESTIVE OF TB OR NOT AVAILABLE

CLINICAL SUSPENSION HIGH

PMDT CRITERIA ,HIGH MDR SETTINGS

MICROBIOLOGICAL- LY CONFIRMED TB

REPEAT CBNAAT ON 2nd SAMPLE

RIF SENSITIVE

RIF INDETERMINATE

RIF RESISTANT

REFER TO MANAGEMENT OF RIF RESISTANCE

SMEAR EXAMINATION

CXR

MTB

MTB NOT DETECTED OR CBNAAT RESULT NOT AVAILABLE

CONSIDER ALTERNATE DIAGNOSIS AND REFER TO SPECIALIST

CLINICALLY DIAGNOSED TB

DETECTED

INDETERMINATE ON 2ndSAMPLE ,COLLECT FRESH SAMPLE FOR LIQUID CULTURE / LPA

• ALL PRESUMPTIVE TB CASES SHOULD BE OFFERED HIV COUNSELING AND TESTING.

CBNAAT

ALTERNATE DIAGNOSIS

Rheumatology

1. Managementoflowbackpain

Low back pain

Presence of sciatica

Yes

Simple back pain- 60% -age under 50

– no systemic disease

– no cancer

Likelihood of musckuloskeletal cause – approx 0.9%

Symptomatic Rx

Improved

STOP

nfection or umour

suspected

Improved

STOP

Symptomatic RX

Not improved

Not Improved

Not improved

Complicated back pain without radiculopathy

– Age over 50yr

– Systemic symptoms/ signs

– Probability of systemic disease 1-10%

– Likelihood of musculoskeletal cause –95%

Radiculopathy – approx 3%

Urgent situations (<1%)

– Acuteradiculopathy

with urinary retention

– Progressivemotor

weakness

– Mayhavesystemic

signs and/or risk factors

Plain film ESR

Urgent consultation with CT/MRI to evaluate for cord or cauda equina compression

I t

Plain X Ray/ ESR

– Ifeitherabnormal,considerCT/MRI

– Highclinicalsuspicioninpatientwith known cancer and new back pain or

patient with fever and backpain

– Closefollowupiswarranted.

Red flag symptoms/ signs

– Age>50yrs

– Systemicsymptomslikefever,chills,night sweats, fatigue, anorexia, weight loss

– h/omalignancy

– nocturnalpains/nightsymptoms

– immunesuppression

– h/oIVdrugabuse

– prolongedcorticosteroiduseorosteoporosis

– trauma

– recurrentskininfection/UTI/genitalinfection

Conservative care for 4-6 weeks if no neurological deficit

2. Algorithmforapproachtomusculoskeletalcomplaint

Musculoskeletal complaint

Non articular condition: consider

– Trauma/fracture

– Fibromyalgia

– PolymyalgiaRheumatica

– Bursitis

– Tendinitis

Yes

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?

Is it articular?

Yes

Is the complaint >6 wks duration?

Acute

Yes

Chronic

Consider

– Acute arthritis like

– Infectious arthritis

– Gout

– Pseudo gout

– Reactive arthritis

– Initial presentation of chronic arthritis

Un Co –

–

Osteoarthritis

Are DIP, CMC1,hip or knee joints involved?

Yes

Chronic non inflammatory arthritis

Chronic inflammatory arthritis

How many joints are involved?

1-3 jts

>3 jts

Is involvement symmetric?

Chronic inflammatory mono/oligoarthritis Consider

– Indolent infection

– Psoriatic arthritis

– Reactive arthritis

– Pauci articular JIA

likely to be OA nsider

Osteonecrosis Charcot arthritis

Yes

– Is inflammation present?

– Is there prolonged morning stiffness?

– Is there soft tissue swelling?

– Are there systemic symptoms?

– Is the ESR or CRP elevated?

Consider

– Psoriatic arthritis

– Reactive arthritis

Chronic inflammatory polyarthritis

Are PIP, MCP or MTP joints involved?

Consider

– SLE

– Scleroderma – Polymyositis

Rheumatoi arthritis

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

• Fever +/- chills • +/-Hypotension

• Urticaria/ Pururitus

• Bronchospasm

• Angioedema

• Hypotension

• No fever

• Respiratory

distress

• Fever +/- chills • Respiratory

distress

• Hypotension

• Fever/chills • Otherwise

asymptomatic

• Fever +/- chills • Hypotension

• Flank/back pain • Bleeding

Sepsis suspect

Urticarial or anaphylactic reaction suspected

TACO suspect

Chest radiography, oxygenation status

TRAIL suspected

FNHTR suspected

AHTR suspected

• DAT (Combos) test

• CBC, Urine dipstick

Supportive data:

• Hypoxia

• Infiltration on

CXR

• Diuretic

response

• Hypertension

• High cardiac

filling pressures

• High NT-proBNP

• Cardiac history

• Older age

• Large infusion

volume

Supportive data:

• Hypoxia

• Infiltration on CXR

• Pink frothy airway

secretions

• Transient

leukopenia

• Onset during or

within six hours of transfusion

Supportive data:

• Lack of any finding associated with AHTR, TRALI, sepsis, or other systemic illness (i.e, Diagnosed of exclusion)

• Non- leukoreduced blood productsHypoxia

Supportive data:

• Hemoglobinemia

• Hemoglobinuria

• Positive DAT

• Low haptoglobin

• High LDH;

bilirubin

• Findings of DIC

• Clerical error

discovered

Supportive data:

• Positive gram stain and culture

• Visibly cloudy product or precipitate

• More common with platelets

Supportive data:

• Urticarial reactions have urticaria alone

• Anaphylactic reactions may have:

• Wheezing

• Angioedema

• Hypotensio

• Low IgA

level; anti- IgA

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

Diagnosis of ITP

Platelet count

< 30,000/microL or

bleeding symptomps

Platelet count

< 20,000/microL or

bleeding symptoms

Platelet count 20,000/microL or

bleeding symptoms

Platelet count

> 30,000/microL or

no bleeding

Platelet count

> 20,000/microL or

no bleeding

Glucocorticoids (IVIG)

Splenectomy, rituximab, or a TPO receptor agonist*

TPO receptor agoinst or combination therapy

Platelet count

> 20,000/microL or

no bleeding

Observe, No treatment

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

Yes No

High-risk MM

Is the patient eligible for autologous HCT?

Standard-risk MM

Is the patient eligible for autologous HCT?

Yes

4 cycles of KRd or VRd followed by stem cell collection and early single or double HCT followed by proteasome-inhibitor- based maintenance

8 to 12 cycles of VRd followed by bortezomib-based maintenance

4 cycles of VRd followed by stem cell collection

Discuss early versus HCT

Is the patient frail?

Early HCT preferred

Delayed HCT preferred No

Yes

Autologous HCT followed by at least two years of lenalidomide maintenance

Start or continue VRd for a total of 8 12 cycles followed by lenalidomide maintenance

Rd until progression

4. ALGORITHM FOR EVALUATING SUSPECTED IRON DEFICIENCY

Typical findings in iron deficiency Medical history may show:

• Symptoms of anemia, pica, restless legs syndrome

• Conditions that could interface with iron intake

(e.g, positive FH for celiac disease: GI syndrome)

• Potential sources of blood loss (eg. Heavy menses, pregnancies, GI bleeding frequent blood donation)

Examination may show:

• Stigma of iron deficiency

• Source of blood loss(eg, occult blood in stool) CBC may show:

• Anemia

• Low RBC count

• Microcytic/hypochromic RBCs

• Low reticulocyte count

• High platelet count

Serum ferritin <15 ng/mL? OR

Serum ferritin <41 ng/mL if anemia and comorbidities present?

Yes

Iron deficiency confirmed

Iron studies panel includes the following:

• Iron

• Transferrin/TIBC

• Ferritin

• Percent transferrin saturation

(TSAT): calculated as iron/TIBC× 100)

•

• Identify source of iron deficiency and/or blood loss

• Treat with iron

Yes

Iron deficiency confirmed

Obtain iron studies*

Transferrin saturation (TSAT) low?

• Identify source of iron deficiency and/or blood loss

• Treat with iron

Additional (specialized) testing for iron deficiency

AND/OR Additional testing for other

causes of anemia or symptoms

Adult with suspected iron deficiency or iron deficiency anemia

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

Yes

Did the patient receive a transfusion within the last four weeks?

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

Urgent hematologist involvement. Possible evaluation for:

• Thrombotic microangiopathy (TMA)

• Acute hemolytic transfusion reaction

• Rapid intravascular hemolysis

Details of the evaluation depend on clinical features and blood smear findings.

Yes

Pursue specific testing based on history, examination and findings on blood smear

Yes

No Negative D

Refer to up to date for available of acute and delayed hemolytic transfusion reactions.

It may also be appropriate to evaluate for other causes of hemolysis.

Is there obvious evidence of an inherited intracorpuscular cause such as lifelong anemia or classic findings on blood smear?

AIHA diagnosed, refer to up to date for distinction between warm and cod AIHA and search for associated conditions.

Positive DAT

Common causes include autoimmune hemolytic anemia(AIHA), drug-induced hemolysis and infections.

Less common causes include hemoglobinopathies, RBC membrane defects, PNH, aortic stenosis and mechanical or osmotic lysis.

Evaluation based on history, examination, blood smear review anddirect antiglobulin (Coombs) test (DAT)

AIHA less likely; other disorders may be suggested by findings on history, examination, and blood smear.

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

PV confirmed

JAK2V617Fnegative

EPO subnormal

Exon 12 mutation identified

Bone marrow biopsy showing hypercellularity for age with trilineage growth (panmyelosis) with prominent erythroid, granulocytic, and megakaryocytic proliferation

Perform bone marrow biopsy and aspirate

EPO normal or elevated

Inconsistent with PV: evaluated for other causes of polycythemia

Bone marrow biopsy not diagnostic

PV: polycythemia vera; EPO: erythropoietin

PV confirmed

Check for JAK2 exon 12 mutation

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

Minor population of Minor population of Microcytic RBCs present Microcytic RBCs present

Anemia detected on CBC

MCV low (<80fL)

MCV normal (80 to 96 fL)

MCV increased (> 100 fL)

Requires additional testing, such as:

• Examination of peripheral smear for abnormal RBCs

• Presence of hemolysis (LDH, indirect bilirubin, haptoglobin)

• Presence of blood loss

• Bone marrow suppression (Low reticulocyte response)

• Renal insufficiency (elevated

creatinine)

Iron studies

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

Other causes:

• Increased Reticulocyte

• Liver disease

• Hypothyroidism

• drugs

• Dysplastic Feature present • Cytopenias

present

Myelodysplastic disorder

• Serum B12 and folate levels

• Methylmalonate (if needed)

• Homocysteine (if needed)

• LowFe

• Normal or

low TIBC

• Normal or high

ferritin

• Normal to high Fe

• Any TIBC

• Normal to high

ferritin

• Low Fe

• High TIBC

• Low ferritin

Iron deficiency determine cause

• Low B12

• Elevated

methylmalonate

• Elevated

homocysteine

• Low folate

• Normal

methyl

malonate

• Elevated

homocysteine

Anemia of chronic disease:

Infection, Inflammation or Malignancy

• Iron overload present

• Siderocytes on

peripheral smear

• Sideroblasts on bone

marrow

• Teardrop red cells

• Target cells

• Splenomegaly

• Positive family history

Alpha or beta thalassemia: perform hem9o3globin electrophoresis

B12 deficiency:

determine cause

Folate deficiency:

Determine cause

Sideroblastic anemia: determine 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

Repeat testing abnormal

aPTT and PT both prolonged

Refer to up to date content on these findings

aPTT prolonged, PT normal

aPTT based mixing study (5 minuted and 2 hours incubation)

Yes

aPTTnormal, PT prolonged

Yes

Evaluation/treatment for underlying problems

PT based mixing syudy and factor VII activity

FVII deficiency

No inhibitor

Testing for intrinsic pathway defects

Prolonged

Normal

Testing for fibrinogen disorders

Testing for common pathway defects

Heparin suspected?

Yes

Evaluation or treatment for underlying problem

Laboratory error, no further evaluation required

Potential cause identified from patient evaluation (e.g, liver disease, DIC, ever- anti coagulation with warfarin)

Potential cause identified from patient evaluation (e.g, liver disease, DIC, ever-anti coagulation with warfarin)

Mixing study does not correct, FVII low

Mixing study corrects, FVII low

FVII inhibitor

Inhibitor present

TT and RT

TT prolonged RT normal

TT normal RT normal

Heparin

Testing based on inhibitor characteristics

Nephrology

ALGORITHM

FOR APPROACH TO GLOMERULONEPHRITIS

Spun urine

Check for dysmorphic RBCs/RBC cast

Yes

Serological tests (C3, C4, ANA, ANCA, ASO, Anti GBM, HBV/HCV, Cryoglobulin), Blood culture

Kidney biopsy (Microscopy + IF)

Haematuria Proteinuria Hypertension Edema± renal failure

No glomerulonephritis

Glomerulonephritis present

Glomerularimmunecomplexes +

Circulating Anti GBM + Linear IgG staining

Lung involvement No

Yes

Low C3 and C4 (Complement mediated)

Normal C3 and C4 (Antibody mediated)

Anti GBM GN

Goodpasture’s GN

SLE (ANA+)

PIGN (ASO+)

Infectious endocarditis

(2D echo and blood culture +) Cryoglobulinemia

(+ Cryoglobulin± hepatitis B/C) MPGN

IgA Immunostain +

Primary GN No

Yes Systemic vasculitis

Yes

HSP

p-ANCA +

Granulomas + Asthma + Eosinophilia +

IgA Nephropathy

ANCA + (Paucity of IF staining)

Granulomas –

c-ANCA +

Wegner’s/GPA

Microscopic polyangitis/PAN

Churg- Strauss/EGPA

2. ALGORITHM FOR EVALUATION OF HAEMATURIA

Visible haematuria

Serum creatinine/eGFR Exclude transient cause including UTI

Symptomatic non-visible haematuria

Non-visible haematuria

Exclude transient cause including UTI

Asymptomatic non-visible haematuria

2 to 3 dipstick tests positive

Yes

≥ 40 yrs

Stop

< 40 yrs

Nephrology assessment

Cause established

Blood pressure

Serum creatinine/eGFR Send urine PCR or ACR

Urology assessment

. Imaging and cystoscopy

Normal All of:

. eGFR ≥60 ml/min and

. ACR < 30 or PCR < 50 and . BP < 140/90 mm Hg

Abnormal One of:

. eGFR < 60 ml/min and

. ACR ≥ 30 or PCR ≥ 50 and . BP ≥ 140/90 mm Hg

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

3. ALGORITHM FOR EVALUATION OF PROTEINURIA

Microscopic urinalysis Negative

Trace to 2+ protein on dipstick test

Repeat urinalysis 2 to 3 times in next month Positive

Positive

3+ to 4+ protein on dipstick test

Findings consistent with renal disease

Negative

Transient proteinuria

Creatinine clearance

Normal

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

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

Normal Age < 30 yrs

Work-up for orthostatic proteinuria

Reduced

Symptomatic Proteinuria

Reduced

Symptomatic Proteinuria

Obvious underlying cause

Cause unclear Obvious cause

Isolated proteinuria

Reassure, no follow up required

Reassure, BP measurement and urinalysis every year

Consider Nephrology consultation

Treat underlying disease

Consider Nephrology consultation

Positive Negative

Treat cause

BP measurement, urinalysis and renal function testing every 6 months

100

ALGORITHM FOR MANAGEMENT OF SNAKE-BITE

Suspected snake-bite

Overt Bite

History of bite nonvenomous (70%)/venomous (30%)

Occult Bite

No history of bite

Krait

Asymptomatic

Dry bite

Symptomatic Predominant symptom manifestation

Viper

Cobra Krait

Myotoxic

Sea snake

ASV

101

. Neuroparalytic symptoms with no local signs

. Severe abdominal pain, vomiting

Anxiety, Palpitations, Tachycardia,Paresthaesia

. ASV

. Atropine and neostigmine (Not to be given in confirmed krait bite)

. Ventilation

Observe for 24 hours

Progressive painful swelling

Neuroparalytic

Vasculotoxic

Russel’s viper Saw Scale viper

. Local necrosis . Ecchymosis

. Blistering

. Painful swelling

. Compartment syndrome

. Ptosis

. Diplopia

. Dysarthria . Dysphonia . Dyspnoea . Dysphagia . Paralysis

. Bleeding

. Demonstrable coagulopathy

(20WBCT incoagulable)

. Shock

. Acute kidney injury

. Muscle ache

. Muscle swelling . Involuntary contractions of muscles

. Compartment syndrome.

. ASV

. Atropine and neostigmine (Not to be given in confirmed krait bite) . Ventilation

. ASV

. Supportive treatment

. Dialysis

. Blood transfusion

. ASV

. Supportive treatment

. Dialysis

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

Evaluation depends on urinalysis

High risk for renovascular disease?

Yes

Evaluate for renovascular disease

Relieve obstruction, if kidney function is determined to be salvageable by imaging or renal scan

Is there albuminuria or RBC cast/ dysmorphic RBCs in urine?

Yes

Evaluate for glomerulonephritis

Sterile pyuria

Evaluate for interstitial nephritis

Follow serum creatinine. Does creatinine remain stable?

Normal urinalysis

Yes

Is there evidence of marked chronicity on imaging?

Yes

102

Kidney biopsy

No further evaluation. Follow closely for renal replacement therapy.

6. ALGORITHM FOR EVALUATION OF HYPONATREMIA Hyponatremia

Serum osmolality

0 00

Volume status

0 00

Hypovolemic Euvolemic Hypervolemic 00

Normal

(280 – 295 mosm/kg)

Hypotonic hyponatremia

High

(> 295 mosm/kg)

Isotonic (Pseudo) hyponatremia

1. Hyperproteinemia 2. Hyperlipidemia

Hypertonic hyponatremia 1. Hyperglycemia

2. Mannitol, Sorbitol, Glycerol, Maltose

3. Radiocontrast agents

Low

(< 280 mosm/kg)

1. SIADH

2. Post-op hyponatremia 3. Hypothyroidism

4. Psychogenic polydypsia 5. Beer potomania

6. Adrenocorticotropin deficiency

103

Edematous states

1. Heart failure

2. Cirrhosis of liver

3. Nephrotic Syndrome

4. Advanced renal failure

UNa+< 10 mEq/L Extra-renal salt loss

1. Dehydration 2. Diarrhoea 3. Vomiting

UNa+> 10 mEq/L Renal salt loss

1. Diuretics

2. Nephropathies

3. Mineralocorticoid deficiency

4. Cerebral salt wasting

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

Address obstruction

Obtain ultrasound. Does it show obstruction?

Yes

Replete volume and recheck creatinine

Did Creatinine return to baseline?

Evaluate for glomerulonephritis

Evaluate for acute interstitial nephritis

Does history and examination suggest volume depletion?

Get urinalysis/microscopy and protein-creatinine ratio

Is there abnormal proteinuria and/or haematuria?

Is there sterile pyuria? Yes

Yes

Evaluate for ATN

Does history/physical examination suggest sepsis, shock/hypotension, or nephrotoxin exposure?

Depending on history, examination and lab investigations, consider less common causes like rhabdomyolysis, tumour lysis syndrome, acute 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

If no apparent cause and creatinine continuously rising or severely elevated, then consider kidney biopsy

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 (Water diuresis)

. Psychogenic polydipsia

. DI (Central & nephrogenic)

. Partial DI (Central & nephrogenic)

. Simultaneous water and solute intake

. CKD

. Hyperglycemia

. Azotemia

. High solute intake

ü IV fluids

ü Enteral and

parenteral

nutrition

ü Exogenous

supplements

Water deprivation test

Uosm = 100-300 mOsm/kg (Mixed Polyuria)

105

Uosm> 300 mOsm/kg (Solute diuresis)

24 hour urine collection (Estimation of osmoles) . Urine sodium

. Urine potassium

. Urine glucose

. Urine urea nitrogen . Other osmoles

9. ALGORITHM FOR RISK STRATIFICATION AND MANAGEMENT OF HYPERKALEMIA

Yes

Serum potassium > 6.5 meq/L

Exclude Pseudology

Yes

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 Glucose-Insulin infusion) in addition to therapies that remove potassium from body (Haemodialysis, Gastrointestinal cation exchanger and/or diuretics)

Is serum potassium > 5.5 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

– —

106

Lower potassium promptly using therapies that remove potassium from body, especially haemodialysis for ESRD patients. Stop ACEI/ARBs, remove any external source of potassium like fruits, juices etc.

Potassium can be lowered slowly by use of diuretics or gastrointestinal cation exchanger. Stop ACEI/ARBs, remove any external source of potassium like fruits, juices etc.

10. ALGORITHM FOR DIAGNOSIS OF HYPERCALCEMIA

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

Elevated

Low normal or low

Measure intact PTH

Primary hyperparathyroidism

If PTHrp elevated; humoral hypercalcemia of malignancy likely

If 1, 25- dihydroxy Vit D elevated; lymphoma, granulomatous diseases (Sarcoidosis, Tuberculosis) more likely

If 25- Hydroxy Vit D elevated; Vitamin D intoxication likely

If none, then measure

. SPEP

. UPEP

. Serum free light chain assay

Multiple Myeloma

Abnormal

Upper normal range or minimally elevated

107

Measure

. PTHrp

. 1, 25- dihydroxy Vit D . 25- Hydroxy Vit D

Primary hyperparathyroidism likely, consider Familial hypocalciuric hypercalcemia

Normal

Assess for other causes like Vit A Intoxication, Hyperthyroidism

BANGALORE MEDICAL CONGRESS

Tags: ALGORITHMS IN MEDICINE

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ALGORITHMS IN MEDICINE

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