Common Questions about Intestinal obstruction (IO)

 1. What are the cardinal symptoms of IO?

-, colicky abdominal pain, abdominal distention and vomiting, no BO, no flatus (obstipation/ absolute constipation)

- other history you want to establish 

• chief complain
• to explore regarding the cardinal Sx
• duration of symptoms
• abdominal pain: to see the location so we can locate either small or large bowel. 
• if its small bowel pain : felt in the upper abdomen and central (periumbilicus) while if large bowel pain is felt in lower abdomen
• these are all visceral pains that is why you referred to area of referred pain

- onset of pain? which one comes earlier? small or large?

• small bowel first
• proximal, smaller in diameter- which would cause distension early, higher level of obstruction 
• small bowel is also active in peristalsis, so once they are obstructed they will cause intense colicky pain. 

- vomiting

• onset : 
• small bowel is active in absorption of nutrients in GI tract. It produces a lot of fluids. If it is obstructed there will be a lot of fluid accumulation so the vomiting will occur early. 
• while in large bowel there is not much of fluid and it is distal, the vomiting occurs late

• content : we will be able to observe the content either from vomiting, or from an NG tube insertion. then we can see the colour content in the bag
• if its feculant material : lower small bowel
• greenish or bile content : high small bowel

Q2. causes of IO and how do you classify

• dynamic
• adynamic
• first we need to rule out mechanical obstructions first
• intraluminal : tumor
• impacted stool: rare, usually in pt with hirchsprung disease
• colon tumor: left sided tumor (Large bowel obstruction)
• small pellet stool, constitutional symptoms, blood in stool
• bowel habit
• PR bleed
• mucous discharge
• tenesmus
• family hx of colon Ca
• intramural, 
• extramural : adhesion, hernia 
• hernia usually affects the small bowel. so if the patient with cardinal symptoms mention above leading towards SBO, remember to confirm regarding their abdominal surgery and hernia. 

Q3. Complications of IO

• perforation
• pain became severe and intolerable
• localised pain became generalised
• presence of high grade fever
• abdomen become more distended

HPB Q&A for HO

HPB = Hepatobiliary

Anatomy of HPB 

Common classifications used in HPB

1. Ranson criteria

2. Mirrizi classification

biliary colic -> acute cholecystitis -> acute cholangitis, pancreatitis, gb empyema and gangrenous gb

presentation of each spectrum

Causes of obstructive jaundice

• 
  
  
  
  

painless vs painful jaundice

• Painful obstructive jaundice is usually related to gallstones, while painless obstructive jaundice tends to be related to tumours.

Q1: If patient came with features of ascending cholangitis, what Investigation you would like to order

• FBC - to monitor TWC, PLT. 
• low platelet: sepsis induces/ severe sepsis that causes coagulopathy
• BUSE - urea, creat monitoring
• hyperbilirubinemia can cause hepatorenal syndrome and renal impairment
• severe sepsis that causes organ failure : kidney failure
• LFT: TB, kiver enzymes and albumin level
• especially ALP and direct bilirubin that can help determin if there are any obstructive jaundice
• ABG: any acidosis or resp failure
• CXR first, as we can use it to rule out perforated viscus
• unless obvious jaundice, so less likely perforated PUD

Q2: why we need ultrasound HBS for ascending cholangitis?

• to rv CBD(common bile duct) size, and any dilatation
• any stone present- if there's obstruction , might need urgent intervention to relieve obstruction
• sometimes stone cant be seen as obscured by bowel gas. 
• stone is usually in distal CBD - the narrowest part
• and it is at the back of duodemun
• usg wave cannot go through gas
• To rule out liver abscess
• as the presentation of liver abscess is the same: RHC pain, fever and jaundice

Q3: normal size of CBD?

• 3-5mm
•  >8mm considered dilated (usually we use >10mm or 1cm as dilated)

Q4: why do we need to rule out liver abscess urgently?

• if huge liver abscess need to drain urgently. 
• gold standard tx: percutaneous drainage and antibiotic
• otherwise it will rupture and cause peritonitis --> severe sepsis --> mortality

Q5. if found out patient have ascending cholangitis secondary to choledocholithiasis, how would you manage?

• resuscitate and stabilize the patient first with ABC
• Airway
• Breathing
• Circulation
• insert branula + blood for Ix and blood culture
• fluid resus
• antibiotics
• analgesia

Q5a. what are the choice of antibiotics use for the pt above?

• HBS common organism are
• function of liver: it uses portal circulation, 
• it collects blood from gut  - all the guy -> return back to liver
• therefore in the GI tract, mainly organism gram negative and anaerobes
• also called BROAD SPECTRUM of negative organisms
• so we need at least 3rd generation cephalosporin 
• eg: cefobid / cefoperazone
• to cover anaerobes: metronidazole

Q6. after analgesics what can we do for patient with ascending cholangitis and in pain?

• if Stable, we can try ERCP to remove the stone . if unable to do so we will put stent to drain the obstruction
• ERCP needs sedation, and prone position. therefore difficult to maintain airway
• If patient is unstable , the option is PTBD

Q7. when to do cholecystectomy?

• once sepsis is resolved
• stone not cleared through ERCP 

Q8. How do you tell which liver segment was it from a CT scan?

Anatomy of liver :

note that 2 is beside 4a, 3 below 2 and 4b is below 4a

upper segment at right side is segment 7,8

and lower right is segment 6 and 7

 First you can check the segments from identifying the hepatic veins. As shown in diagram above, left hepatic vein separates segment 2 and 4a, then the middle hepatic vein for segment 4a and 8, right hepatic vein for segment 8 and 7

Then as you scroll down the ct scan, you will see the portal vein (left branch). the portal vein separates the liver to the left(segment 2 and 4a) and right side (segment 7,8) . below the portal vein emerges segment5

When you can see the right branch of portal vein, it also indicates that on Left (segment 4b, and segment 3), on its right is segment 5 and segment 6

reference, more on website: 

1. https://radiopaedia.org/cases/liver-segments-annotated-ct-1

2. https://radiologyassistant.nl/abdomen/liver/segmental-anatomy

Electrolyte Imbalance QnA for HO

 House Officers must know in ward 

- Electrolyte imbalance

Q1: 50year old, 70 kg, male with persistent diarrhea and vomiting for 3days due to food poisoning. He is dehydrated. Vitals are stable, looks lethargic. Na: 128mmol/L

a. How to correct his hyponatremia

    - calculate first

• Na deficit (mmol) : (desired Na level - serum Na) x bw x fraction
• 0.6 x kg x (desired Na - serum Na)
• desired Na :  135-145
• Na deficit is 0.6 because extracellular comprises 60%. 
• If its potassium (intracellular) therefore 0.4 cause it is 40%
• 0.6 x 70 x (135-128) = 294mmol/L

    - to add with daily requirement

• infusion = deficit + requirement
• requirement: 1-2mmol/kg/d (we usually use the lower range when calculating)
• infusion: 294 + 70 = 364 mmol/L

- then how do we deliver 364mmol/L to pt?

• 1 pint NS = 77mmol/ L
• 1L NS = 154mmol/L
• 364 / 77 = 4.7 pints, 
• therefore 5 pints of normal saline over 24 hours is needed.

b. the next day his repeated Na is normal: 136, 

how do you plan for fluid regime ? for maintenance?

• normally a person need 30-40ml/kg/d (fluid requirement)
• general normal weight for man: 70kg,  normal weight for woman : 60kg

• if we take the middle value fluid requirement (35ml/kg/d), 
• the man will need 2450ml (around 5 pint as well)
• women is 2100ml, around 4pint. 

thats why usually we see usually 

• 5 pint (2/3 pint NS + 2/3 pint D5%) given to man, 
• 4 pint(2 pint NS + 2 pint D5%) given to women. 

** WHY 2 or 3 pint NS? for example a 70kg man we take 140mmol Na requirement, 1 pint NS is 77mmol, therefore the man only need 2 pint NS. but his fluid requirement is 5 pints a day, that's why we need to add another 3 pint D5 to complete his daily fluid requirement. 

Q2. what should you watch out during sodium correction?

• Na correction should not exceed 10mmol/L/24 hours
• thats why we use the lower normal when correcting sodium
• even in severe hyponatremia, if Na only 120, your aim of correction is only up to 130, and not up to 135 in 24 hours. 
• if there are hypernatremia (rare), mostly we try to find out the associated conditions/ related underlying issues. usually will be given diuretics to excrete excess sodium. 

Q3: 50year old, 70 kg, male with persistent diarrhea and vomiting for 3days due to food poisoning. looks lethargic, no ecg changes.  K: 3.2mmol/L

a. how to correct his potassium?

• Deficit = (desired K - measured) x Body Weight (BW) x 0.4
• (3.5-3.2) x 70 x 0.4 = 8.4mmol
• 70 for maintanence , 
• maintanence + deficit = infusion
• 70+8.4 = 78.4
• 78.4/13.3 = 5.8gm
• we take normal daily requrement of K : 1mmol/kg/d, therefore we need to convert into gm  by dividing 13.3
• 1gm = 13.3mmol
• so we need to correct at least 5 gm first
• can correct with 1g KCL in each pint NS (total 5gm)/24hours

b. what is the maximum/ safe dilution of K+ in 1 pint of NS?

• dilution cannot exceed 40mmol/L
• which also means cannot exceed 20mmol/pint = 20/13.3 = 1.5gm KCl
• we cannot give more than 1.5gm KCl in a pint of NS

c. what is the safe titration of K+?

• titration of potassium cannot exceed 10mmol / hour
• if we need fast correction due to symptomatic, 
• max is 1gm KCl in 100cc NS over 1 hour, not faster than that

• If need 2gm infusion, it must be in 2 hours.
• never bolus correction, must always use safe titration
• 2gm KCl infusion in 200cc NS over 2 hours

• OTHERWISE can cause CARDIAC ARREST! 

Q4: How do we know the patient has hyperkalemia?

• Cut off point for hyper K: 
• K+ > 5.5
• symptomatic ECG changes: tall tented T waves, absence of P wave, broad QRS, PR prolong
• it became dangerous when the ECG changes go towards heart block type of ECG with tall tented T wave --> severe hyperkalemia --> lead to arrythmia then asystole

Q5. what is the fx of each components in lytic coctail? 

• lytic cocktail: treatment for hyperkalemia
• Calcium gluconate - 10ml 10% calcium gluconate
• for cardio protection
• Insulin / actrapid 10u : 
• drive K+ into cell together with glucose
• Glucose/ D50 - 50ml : 
• K+ transporter
• we need to administer calcium gluconate follow by insulin then D50

Q5a. so why we cannot give insulin first instead of glucose?

• Potassium cannot enter the cell by itself, thats why we need glucose first ,since it is the transporter it can allow the insulin to drive the K into the cell. 
• GLucose is the transporter
• so we need to load the excess potassium onto the glucose
• Insulin cannot push the K directly, they need transport. therefore they need glucose first, then insulin will push both into the cells. 

Q5b. how many times can we give lytic cocktail?

• every 6 hourly
• if the potassium is still not corrected, Hemodialysis (HD) is needed

But we could not just correct potassium with just lytic coctail,  have to correct the cause of hyperK as well. 

Q5c. what are the common cause of HyperK in surgery?

• Acute Kidney Injury (AKI)
• severe dehydration, sepsis can cause AKI. 
• If there are evidence of sepsis, we need to find the source and remove its source of infection
• antibiotics
• If there are acidosis, we need to find the cause and solve it from there as well. 

Q6. what are the common antibiotics used in Gastrointestinal - GI sepsis?

• cefobid and flagyl

• common organism in GI
• gram negative : E.Coli, Klebsiella, Enterobacter
• GI accomodates a broad spectrum of gram negative organisms
• anaerobes

• 1st generation of cephalosporin covers gram positive
• exp: cephalexin
• 2nd generation covers gram positive and a bit of gram negative (narrow spectrum)
• cefuroxime
• 3rd generation covers broad spectrum of gram negative
• cefobid/ cefoperazone

• Metronidazole: covers anaerobes

• If patient has carbuncle, abscess or soft tissue infection / sepsis, the choice of antibiotic should be covering skin organism: 
• empirical antibiotic
• penicillin based: cloxacillin, etc. 
• for Urology patient, usually have narrow spectrum of organism, 
• common: E. Coli
• can use cefuroxime as empirical antibiotic, unless they have sepsis, so may need to consider quinolones to cover for broader/ other pathogens

Q6a. so when do we change antibiotics? 

• observe if antibiotic works, after 3-5 days
• usually the patient will show clinical improving and total white cell count (TWC) will reduce
• but if no changes after 3 days, we might need to consider changing to a higher efficacy antibiotic
• 
  

Fluid and Resus common QnA for HO

Part 1: Fluid and its components

Q1. What are the common cause of fluid loss in surgery?

• apparent loss: diarrhea, vomiting and high output stoma
• 3rd space loss: 
• loss of water, electrolyte and colloid particles into interstitial space
• which could contribute to edema
• Intestinal obstruction, pancreatitis and ascites
• others: insensible fluid loss (hyperventilation/pyrexia), stress response

Q1a. How patient loss fluids from IO?

• apparent loss: vomiting
• 3rd space loss: 
• increased secretions
• bowel obstruction will cause bowel to secrete a lot of secretion to overcome the obstruction. 
• mucosal edema, so fluid not absorbed
• so there will be a lot of accumulation of fluid that leads to third space loss
• fluid accumulation in bowel can reach up to 6L
• that could lead to hypovolemic shock

Q1b. How patient loss fluid from pancreatitis?

• systemic inflammation 
• inflammation causing release of inflammatory cytokine and other pro-inflammatory mediators,
• leading to capillary leakage
• thus loss of circulatory albumin and fluids to interstitium
• capillary leakage cause fluid shift to third space and then hypotension leads to hypovolemic shock.

Q2. What is the main difference between crystalloid and colloid?

• molecular size
• affects shifting of fluid where low molecular size - low tonicity

Q3. How does fluid moves in human body?

• from low concentration to high concentration 
• big molecules fluid (colloids) 
• has ability to pull fluids from other compartments : oncotic pressure
• opposite of oncotic pressure: hydrostatic pressure

** not through pressure gradient / osmosis

Q4. What is isotonic?

• a solution concentration that is similar to plasma
• the osmolarity of plasma is around 300 mosm/L
• Normal saline: 308
• Half saline: 154 (hypotonic)
• 3% saline: 1026 (hypertonic)

Q5. What is the difference between Normal Saline (NS) and Hartmann(HM) solution?

• Hartmann has additional potassium, lactate, calcium
• the most "physiological" solution

Q5a. What is the function of lactate in HM

• lactate will be metabolised by liver to HCO3, thus acting as buffer
• especially in met acidosis

Q5b. Can we use HM as resuscitation fluid?

• No
• usually when patient needs resuscitation, already with multiple organ failure or impairment
• so although Hartmann has lactate that could help as buffer, the liver is unable to convert lactate to bicarbonate, which could lead to accumulation
• the accumulation of lactate will worsen the metabolic acidosis
• and Pt in acidosis usually has hyperkalemia, Hartment contains K+ which would further worsen the situation

Q5b. So when do we use hartmann?

• as maintanence, especially in those who need replace electrolyte loss (diarrhea and vomiting)

Q6. What is the function of Dextrose 5%?

• provide hydration
• the have glucose in solution not for calorie to avoid lysis and avoid hypotonic
• calorie in D5: 170/L
• it is just to render solution isotonic once infused in the circulation, once they reach liver will convert into free fluid
• - provide free water that can pass through membrane pores, expanding both intracellular and extracellular spaces

Part 2: Fluid and resuscitations

Q7. 60year old, 70kg man presents with diarrhea and vomiting for 1 week. brought in with hypovolemic shock
Outline your management for this man

- ABC

• assess airway
• breathing
• circulation
• check the vital signs: unstable/ stable

- insert 2 large bore needles and give IV NS

- run fast 1 pint NS

Q7a : If patient doesn't respond to fluid resus? 

• reaccess: if the volume is improved, but patient still hypotensive, he might have other component of shock
• for example: septicaemic shock --> we might need to start inotrope for vasoconstriction
• if cardiogenic shock / has underlying IHD --> get an ECG, and we might need to start with dopamine or dobutamine as the inotropic support. 
• if volume is still low, 
• can infuse COLLOID to hold the fluid in the circulation
• colloid has oncotic pressure that will hold the fluid intravascularly, thus maintain the BP

• So why we cant give colloid straight away for resus?
• Colloid causes shifting of fluid out of the cell, worsen the hypoperfusion
• in shock, circulation fails and tissue is hypoperfused, if we infuse hypertonic solution all fluid will move from the tissue into the intravascular system . 
• Therefore load with volume first (crystalloid)
• resume the circulation
• let them reach the heart, brain and kidney
• after that infuse colloid to hold the volume. 

Q8: Define shock

• must have 2 components
• circulatory failure: seen via vital signs
• inadequate tissue perfusion : seen via low SPO2
• sequelae of low perfusion
• multiorgan failure

Q9: Why we cant have central line when patient is in shock?

• it is about the catheter's caliber. the shorter the calibre, faster the infusion. 
• if central line, it has long calibre and the rate of infusion is slower
• insertion takes a lot of time
• in shock we need large supply of fluid for the patient 
• Poiseuille law

Q10: How do you know patient responded to your fluid resuscitation? what are your AIMS?

• vital signs 
• HR <90
• BP >90/60 , MAP >60
• SPO2 >95%
• RR <20
• u/o  >0.5ml/kg/hr

UGIB Q&A

 Q1. What is the anatomical level to ddx upper and lower GI bleed?

• at the duodenal-jejunal junction at the ligament of treitz
• UGIB are bleeding proximal to ligament of trietz
• LGIB can also cause from bleeding of small bowel, 
• those bleeding distal to the ligament of treitz can consider as lower GI bleed

Q2. What are your aims in assessment for a patient with UGIB?

• to assess if patient is stable
• if they are in active bleeding
• is it variceal or non variceal bleed

Q2. How to access the stability of the patient?

• vital signs
• mental status
• urine output. 

all these could help chart the grade of shock clinically - especially Heart Rate !

- if you notice from the table below. 

• the heart rate could already classify the type of shock into class I and class II and it also shows us "THERE is BLEEDING" 
• BP came 2nd as when we realise BP drop, shock is already grade 3. 
• and blood loss has already reached at least 1.5L
• if grade 2 systolic pressure is still normal and diastolic is low : 

Q3.  How do we access if they are still actively bleeding?

• colour of hemetemesis
• fresh blood
• coffee ground colour

• amount of hemetemesis
• large?

** anemic Sx is not enough to diagnose if they are still having active bleed. as acute bleed will cause collapse first even before they have the symptoms. 

Q3a. If patient has history of melena, is it usually active bleed or already stopped?

• Yes, usually it is active and has maroon colour, also called fresh melena 

• Blood is irritative to gut, they either comes out from the mouth or the anus. 
• opposite to fresh melena is old melena or stale melena
• Old melena: black is colour, and towards formed stool. 

Q4. Some of the black stool presentation still could be active bleed, what type of presentation we can see in this type of patient?

• large amount of black stool and watery
• also called watery melenic stool 
•  patient family/ Staff nurse can have complain of patient changing diapers multiple times however soaked. although it is not red, still considered active bleed. 
• can happen in both UGIB and LGIB

Rule out UGIB first as 80% of PR bleed is from upper GI, 20% from LGIB

•  Despite resuscitation, patient still has persistent tachycardia

Q5. How to access the source of bleeding, variceal vs non variceal?

• Patient's History
• variceal bleed: large amount of fresh hematemesis, has copious blood
• usually described as bowls of blood or cups of blood. 
• massive bleeding usually came from varices
• however it is usually PAINLESS
• causes:
• any history of liver disease: jaundice, stigmata of liver disease, portal hypertension secondary to chronic liver disease, hep B
• high risk behaviour
• non variceal bleed: cause is usually peptic ulcer disease (PUD)
• pain 
• have hx of epigastric pain
• cause: 
• long standing NSAIDS usage/ steroids usage
• hx of hyperuraemia (CKD)

Why do we need to differentiate variceal and non variceal bleed?

• variceal bleed: need urgent OGDS (no active bleed)
• non variceal still can wait and scope within 24 hours 

Q1: if patient is suspected with variceal bleed, he has active bleeding and continuously vomit blood. 
his vitals are not stable. Outline your acute management

• ABC
• A: If airway compromise to intubate , to secure airway
• insert 2 large bore IV cannula
• blood taking(FBC+coag) + GXM + safe O blood (preferably cross match blood)
• fluid resus with crystalloid then add colloid while waiting for blood and blood products
• can refer to the fluid and electrolyte QnA link here
• to arrest and stop the bleeding
• inserting sengstaken tube

• vital signs monitoring

THEN SEND pt to ICU once he is stable

since patient having active bleed, he is not fit for OGDS, as we couldnt view the source of bleeding clearly. the active bleed will obscure the lens of OGDS

** differences between UGIB 2 to PUD , pt who has variceal bleed, you will need urgent OGDS as long as they have no active bleed. those with UGIB 2 to PUD we still can wait and scope within 24 hours. 

Q1a: what do we do next once patient in ICU- medical therapy?

• start IVI octreotide
• on pt with and without active bleed. 
• replace blood loss and correct coagulopathy
•  FFP
• start antifibrinolytic agent eg: IV tranxenemic acid 500mg TDS
• transfused if needed
• start PPI infusion
• reduces mortality in variceal bleed
• due to reduce in acid in stomach, it also lower down incidence of rebleeding 
• start antibiotic
• as pt usually immunocompromised due to hepatic failure
• in various study shows abx may reduce mortality rate in bleeding pt
• 
  
• beta blocker
• usually given after patient recover
• as might cause low systemic blood pressure in acute setting

Q2: how does octreotide help with the bleeding?

• it inhibits release of glucagon 
• glucagon is splanchnic vasodilator
• when splanchnic circulation is reduced it will cause reduce in portal pressure

Q3: how long can we place the sengstaken tube?

• 48hours
• longest: 72 hours/3days
• as it is just a temporary solution to the problem. 
• however have to deflate the esophageal balloon intermittently every 2 hours
• important to reinfate to prevent hypoxia and necrosis of compressed tissue
• and esophageal perforation is fatal cause it is in the thoracic cavity if perforated. 

Q4: what is the PPI infusion that is given

• IVI pantoprazole 80mg stat then 8mg/hr
• GOLD STANDARD to give the regime stated above. 
• if no pantoprazole, omeprazole is also accepted

Q4b: why PPI is important and superior as medical treatment?

• proton pump inhibitor, blocks the H+/K+ ATPase
• inhibition is irreversible. 
• therefore causes profound and prolonged reduction of acid production

CPG malaysia for UGIB mx

do review back the summary done last time and come test yourself here!'https://yu4med.blogspot.com/2021/04/ugib.html

HO medical - EMERGENCY management

Some of the notes seniors passed down which is very useful. I edited and add in some points i get during my posting as well. 

Big thumbs up to them who prepared the list and Thank You💕💖

1. Hypokalemia
2. Hyperkalemia
3. Hypoglycemia
4. Hyperglycemia
5. Chest Pain
6. Hypotension
7. Asystole
8. VT
9. Atrial Flutter
10. SVT
11. Fit
12. GCS drops
13. Aggressive behavior
14. Nausea/ vomiting
15. Diarrhea
16. Hematemesis
17. Shortness of Breath
18. Other electrolytes
19. UGIB
20. Anaphylaxis
21. Dengue

1. Hypokalemia (K+ <2.5)

- ECG STAT to look for hypokalaemic changes, check whether patient symptomatic.

- 1g KCL in 100cc NS in 1 hour

                or

    2g KCL in 200cc NS over 2hour (according to K+ level)

- with continuous cardiac monitoring

- Add KCl in drip (if patient on drip), mist kcl 15mls tds OR T. slow K 600mg/1.2g OD

- Check TFT, RP, VBG, UFEME

- Monitor v/s

- ECG (any ecg changes)

- Inform MO stat if symptomatic

- Off potassium supplements once K+ >4

- Repeat RP 1 hour post correction

- Daily RP until K+ stable

     

 2. Hyperkalemia (K+ >5.2)

- ECG STAT to look for hyperkalaemic changes, check whether patient symptomatic

- Off potassium supplements

- To serve lytic cocktail 

(10cc of 10% calcium gluconate in 10 minutes - slow bolus with cardiac monitoring + 50cc D50% glucose + 10 unit actrapid)

- If still high, repeat lytic cocktail 

Peritoneal dialysis?? Haemodialysis??

- T. kalimate 5-10g TDS

- Off kalimate once K+ <5

- Repeat RP 1 hour post correction

- Monitor RP daily till stable

3. Hypoglycemia (Reflo <4)

- Omit insulin

- Encourage patient to take orally (sweets, bread with jem, milo)

- If too low (<3.5) with symptoms, give 20-50cc D50% then repeat reflo 30mins

- If reflo 4-6, half the dose of next insulin

4. Hyperglycemia (Reflo >12)

- Serve S/C 6-10 unit actrapid STAT (depends on reflo) if patient not on insulin/insulin served earlier on.

- If patient already on insulin and not served yet, to serve usual dose.

- If persistently high despite insulin to start top up regime based on BMI. Take VBG, lactate and urine ketone dipstick TRO DKA.

5. Chest pain

- ECG STAT.

- If suspected ST elevation, to inform MO for referral to cardio KIV thrombolyse.

- S/L GTN, maximum 3 times. If persistent pain to start IV morphine with IV maxolon. If pain persists despite morphine to start IVI GTN.

- Oxygen

- Aspirin crush 300mg, Plavix 75mg

- Take cardiac enzymes(CK) and Trop T as baseline, to repeat at 6 hours later with ECG

6. Hypotension

- Determine cause (Septic, hypovolaemia, cardiogenic etc)

- Repeat manual BPx2 first to confirm

- Run 1 pint (250cc) NS fast 15-30minutes

     if no contraindication (watchout if patient have ROF).

     If still low, for another try.

- Inform MO is persistently low, KIV start IVI noradrenaline and adjust accordingly

- Regular BP monitoring (ideally every 15mins)

- KIV Gelafundin (colloid) @ inotrope

- Grey branula at neck/femoral line

- IV Noradrenaline 0.2mcg/kg/min

- KIV add another intropes if low despite high dose 1st intropes

7. Asystole

- Inform MO and call CRASH 

- Prepare Resus trolley and intubation kit

- Manual bagging 15L/m (even for ventilated patient)

- Straighten bed and commence CPR

- Transfer to acute bay

- Vital signs, reflo and cardiac monitoring

- Insert 2 large bore branula at least green at big veins (femoral/neck/cub fossa) and take all routine bloods including ABG, reflo and cardiac enzymes (run urgently)

- Run 1 pint NS fast if no contraindications

- Prepare IV adrenaline (1mg every 5 mins 3 cycles)

                IV Atropine 1mg every 3-5 mins (3x)

- If patient survive,

•     take ABG post intubation,
•     ECG,
•     septic workup (if infection is suspected),
•     D dimer (if PE is suspected)

- Keep BP >90/60, MAP >60.

- Insert CBD and strict IO monitoring (Keep U/O > 30cc/hr)

- Start inotropes if low BP

- IV panto 40mg OD to prevent gastric ulcer

- Insert Ryles tube, KIV start feeding later (refer to dietitian)

8. VT

- Inform MO

- Prepare resus trolley

- Vital signs and continuous cardiac monitoring

- If pulseless, for defib and 5 cycles of CPR. Repeat if unsuccessful.

- If pulse present but hemodynamically unstable, for urgent cardioversion and IV

lignocaine

- If pulse present, for IV amiodarone

9. Atrial flutter

- Inform mo

- Vital signs and continuous cardiac monitoring

- If hemodynamically unstable, for urgent DC shock and rate control meds.

9a. Fast AF

- Nasal prong O2 (NpO2)

-Continuous cardiac monitoring

- IV Digoxin (if HF) 0.25mg every 2hr, up to 1.5g within 24hr

- Metoprolol 25mg/100mg BD (absence of HF)

- KIV IVI Amiodarone 300mg over 30mins

- KIV cardioversion if hemodynamic not stable

>10. SVT

- Inform MO stat

- Vital signs monitoring and continuous cardiac monitoring

- If hemodynamically unstable, for cardioversion

- If stable for carotid massage (if no bruit) dan valsalva maneuver

- If persistent, need to give IV adenosine 6mg and flush with 20cc NS.

• then 12mg then 12mg
• if not reverted, IVI amiodarone 300mg over 30 minutes

Contraindicated for Asthma patient.

• Second bolus 12mg can be given after 5 mins with NS flush.

- If persist consider another drug (verapamil etc)

11. Fit

- Remove patient from dangerous objects

- Prepare IV diazepam 5mg STAT, if persist repeat dosage (max 3 doses with 10 mins gap)

- Put on HFM 10-15L/min

- Vital signs monitoring

- Put patient on left lateral position

- If fit persist, KIV IV phenytoin (loading and maintenance)

- Repeat bloods including electrolytes, KIV for CT brain/ LP

- If resolve, continue vitals monitoring, fit charting, - GCS charting

12. GCS drops

- Vital signs and reflo

- Inform mo

- Transfer to acute bay

- Refer CRASH KIV for intubation

- Determine cause

- Insert line and repeat bloods including ABG, septic workup Request for CT brain

-Treat according to cause

13. Aggressive behaviour

- Approach calmly

- Ask help from security guards or male staff

- IV haloperidol 5mg STAT

- 4 points restraints

- Repeat bloods TRO causes

- Refer psych if persistent aggressive behaviour

14. Nausea/vomiting

- IV maxolon 10mg STAT

- Start ORS

- If significant loss, start IVD maintenance

- Monitor RP

- Find the cause

15. Diarrhea

- ORS per purge

- KIV lomotil

- If significant loss, start IVD maintenance

- Monitor RP

- Find the cause

16. Hematemesis

- Inform MO

- Rule out UGIB (inspect vomitus)

- PR examination to look for melena

- Vital signs (look for compensated or decompensated shock)

- If significant blood loss to insert 2 large bore branula and repeat bloods

- IV tranexamic acid 1g STAT and 500mg TDS, IVI pantoprazole 8mg/hr.

17. SOB

- Examine lungs, check vitals

- Determine cause, repeat CXR if needed

- Refer CRASH if necessary (SpO2 unable to maintain with oxygen

supplementation or clinically worsening SOB)

- If intubated, check if ETT dislodged or too deep (if yes, to readjust)

- Start ocygen supplementation (according to SPO2 and clinical). If known case of

COPD to start VM.

- Watchout for respi distress, keep SpO2 >95%

- If significant SOB with Sp02 drop, take ABG, FBC (TRO anaemia), Cardiac

enzymes, Trop I (ACS is suspected), D dimer (TRO PE)

- If ronchi (asthma) - Neb AVN STAT, IV hydrocortisone 200mg STAT (if moderate

to severe). Reassess post neb, if worsening can try back to back neb.

- If PE is suspected, to take D- dimer KIV CTPA. Chest referral, KIV start clexane

- If pneumonia (HAP/aspiration) is suspected, to take septic workup and CXR and

start antibiotics.

- If fluid overload, to serve IV frusemide 20mg STAT (to check BP before serving),

adjust IVD and fluids intake

- If pleural effusion, KIV for tapping

>18. Other electrolyte deranged management

• Hypomagnesaemia:
• IVI MgSO4 1 ampule in 100cc NS over 1 hour
• Hypocalcaemia:
• - ECG
• - IVI CaCO3 1 ampule in 100cc NS 
• over 1 hour @
• - IVI Calcium Gluconate 1 ampule in 
• 100cc NS over 4 hours
• * Mild: Tab CaCO3 500mg BD/TDS

• Hypophosphatemia:
• - IVI KH2PO4 1 ampule in 100cc NS 
• over 4 hours

• Hyponatremia:
• - If no ROF, give IV drip NS 3-4  pints/24 hour

19. Upper GI Bleeding:

- 2 large bore branula 

- Run fluid 

- FBC, Coag profile, GXM 4pint blood

- IV Pantoprazole (PPI) 80mg stat 

and IVI 8mg/hr

- Inform MO

20. Anaphylaxis:

- IV Hydrocortisone 200mg

- IV Piriton 10mg

- IV Maxolon 10mg stat & TDS

- Oxygen 

- IV fluid

- If BP drop,IV/IM Adrenaline 1:1000

21. Dengue1:

- Dengue fever day __, __ warning signs, in __ phase (if defervescence phase point taken at__˚C), V/S, on drip __cc/kg/H, latest FBC reviewed. -

- Next FBC at __am/pm, cont drip __cc/kg/h

* WARNING SIGN: 

- Tender liver - Abdominal pain

- Mucosal bleed

- Persistent vomiting ≥3x + diarrhea  ≥3x/24 hr 

- Fluid accumulation(ascites/pleural E)

- Restlessness/altered conscious level

- Inc haematocrit, reduced platelet

Dengue2:

- N haematocrit: Male: >45; Female: >40

- Raised haematocrit in active smoker & obese pt is normal

- If pt took PCM, take Temp > 6hours after that, to count defervescence phase (< 38˚C)

- Dengue IgM & IgG positive high risk DHF (If systemic bleeding, give IV Traxenamic acid 500mg TDS)

- Ideal Body Weight in Dengue: 

Male: (Ht-152.4) x 0.91 + 50

Female: (Ht – 152.4) x 0.91 + 45