Disclaimer: This is a little collection of ward tidbits that represent my personal opinion. Many things may be contrary to what is taught in medical school or even what your registrars do or want you to do. As such they do not constitute professional advice and should not be viewed as authoritative. Regard them all with a pinch of salt.
Each tidbit should be viewed as a starting point to look things up further rather than a direct recommendation.
Mostly these tidbits are backed up by relevant literature, however it is too tiresome to reproduce this below. If you have a burning desire you can PM me and I will see if I can find the references.
I have grouped them into hopefully sensible headings. Not alphabetical unfortunately.
Feel free to reply and add your own.
The heart
The patient on the ward who develops central chest pain has to be pretty exceptional to not warrant a troponin.
Learn about the STEMI equivalents. These are ECG findings that do not have ST elevation but require emergent PCI nonetheless. Hyperacute T waves and de Winters waves are two such examples. Wellens waves while not necessarily needing emergent PCI do signify a high risk of progressing to an anterior infarction.
In the vein of the above ischemic ST depression is diffuse. Localised ST depression should be viewed as reciprocal to ST elevation elsewhere until proven otherwise. If there is localised inferior depression, look at the lateral leads- a high lateral STEMI can present with only STE in aVL. Similarly ST depression in V2-4 is a posterior STEMI until proven otherwise- do posterior ECGs.
Diffuse ST depression with ST elevation in AVR can be a portender of left main occlusion and always warrants showing a medical registrar (or cardiology if there’s one around!)
T wave inversion is a sign of reperfusion not active ischemia. Flat t-waves, while often ignored, carry the same significance as t wave inversion.
Contrary to popular belief you can diagnose ischemia in a LBBB. Look up the Scarbossi criteria.
People can have ischemic chest pain that does not produce a troponin rise. However if someone has ischemia lasting several hours then this should produce a troponin rise.
Pain radiating to the right arm has proven to be more specific for an MI than pain radiating to the left arm.
What the patient tells you about this pain being similar or dissimilar from their previous MI is largely irrelevant. One study showed “pain similar to previous MI” was actually a predictor of non-ischemic chest pain.
People without obstructive CAD can still have MIs- plaque of any size is capable of rupturing.
Intracranial pathology can produce ischemic ECG changes and troponin rises- always discuss with a senior first in someone who has had an intracranial event before starting ACS treatment.
Heart failure can be subtle and does not necessarily present with overt crackles and edema. If in doubt a BNP is useful – if it is negative. BNP is sensitive but not specific.
Be cautious with frusemide- it is easier to give more than undo the kidney injury you have caused. 5mg IV may produce significant diuresis in a frusemide naïve patient, while in someone with significant CKD, 40mg may barely touch them. It is not good enough to give the frusy then walk away. They should become polyuric in the next few hours and if not, the dose isn’t enough.
It is really easy to iatrogenically overload patients and the likelihood is high you will do it within your first 6 months.
I am yet to meet heart sounds that weren’t dual. This is true even in the BMI 65 patient who leaves you tapping the diaphragm of your stethoscope in a perplexed manner. I have concluded that people are simply too embarrassed to document that they couldn’t hear the heart.
For some reason there is high frequency of coronary events at night (a literature proven phenomenon). Something to do with sympathetic surges during REM sleep.
Lungs
An ABG makes you feel like you are doing something useful but rarely adds a lot in the majority of instances it is done. If you ABG a desaturating patient you will find, surprise surprise, hypoxia. Except now you start to panic because a PO2 of 6.5 looks scarier than a saturation of 88%, but in reality they may be one and the same. You should always be looking for something specific on it, that you can’t get at the bedside, for example CO2. If you don’t care about the CO2 and only want the pH, bicarb etc. a venous gas will do the same job and is far less painful for the patient.
A normal respiratory rate in someone with respiratory distress is concerning rather than reassuring as it suggests they are about to tire.
You cannot make a chronic CO2 retainer stop breathing by giving oxygen. You can drive up their CO2 but this is dependent on the saturations i.e. exceeding 88-92, rather than the flow rate on the wall.
Learn to talk in FiO2 where it is measurable.
Asthmatics should have a respiratory alkalosis on their gas- a normal CO2 is concerning and a high CO2 is terrifying. Going off the above- terror is a legitimate reason for an immediate phone call to a senior.
A talking, alert, oriented patient is a lot less likely to be in acute CO2 retention.
Wheeze is not specific for COPD. Heart failure can give you wheeze. PE can give you wheeze. A lot of things can give you wheeze.
Similarly a COPD patient with an exacerbation may not necessarily have a wheeze until you improve their air entry. Don’t discount COPD based on the absence of a wheeze.
While you won’t be making changes to BiPAP, it is useful to know what IPAP and EPAP are and how they can be changed to affect oxygenation and ventilation.
Salbutamol causes a high lactate-which doesn’t need anything done about it.
PE doesn’t read the textbook. A lot of things don’t, but I feel this is especially true of PE. Don’t regard the Wells criteria as gospel.
You don’t develop an aspiration pneumonia straight away. You develop a chemical pneumonitis. The infection may or may not develop in several days.
What goes on in the abdomen affects respiratory mechanics almost as much as what goes in the chest.
Abdomen/surgery
A lot of examination manoeuvres are taught in depth but generally useless. The abdomen is poorly taught but very very useful. Feel a lot of abdomens in medical school. Train yourself to look closely for scars every time you looks at the abdomen (oh yes I forgot I had my spleen out in 1969).
Normal bloods reduce the likelihood of appendicitis, diverticulitis, etc. They don’t rule them out however. Neither does lack of a fever. This is especially true at the extreme ends of age. A significant proportion of the elderly may have abdominal pathology but normal bloods.
I can count on one hand the number of spleens I have felt in my life.
Bulging flanks (a simple end of bend observation) is more sensitive for ascites than shifting dullness. Don’t believe the hype.
No matter how much radiology objects an ultrasound should always be sought before draining ascites. This becomes apparent when everybody, including the consultant, comments on the gross ascites only to discover that actually the patient is probably just really fat. Do you trust your own examination enough to go blindly sticking needles?
It turns out the adage that people with appendicitis don’t keep eating has been debunked several times. This won’t stop consultants from commenting that the patient probably doesn’t have appendicitis because he’s munching on KFC.
Fever within the first 1-2 days post op is common and if the patient is clinically well and examines normally does not need investigating.
Urine output is unreliable post op as the stress response to surgery causes an antidiuresis. Some sources suggest 0.2ml/kg/hour is normal. Don’t give fluid based solely on a urine output. Positive fluid balance is associated with increased risk of anastomotic breakdown etc.
In fact it seems the less you touch your patients postoperatively the better they do.
Always suspect ischemic bowel in someone in heaps of pain, but who is not very tender. A lactate is useful however a normal one is not necessarily reassuring. For some reason HD patient are at really high risk of ischemic bowel.
After acute bleeding the Hb may initially remain stable. It takes a few hours for the “autotransfusion” of fluid shifting from interstitial to vascular space, thereby diluting haemoglobin.
Don’t trust an Xray to tell you about constipation. Also it is normal to have feces in the colon on Xray- that is the purpose of the colon! If you’re doing an Xray to look for faecal loading you need to stop being lazy and do a rectal!
Don’t lie to the patient by telling them “this rectal won’t hurt”. Better to be honest.
Remember there are non-surgical causes of abdominal pain. Chief not to forget are MI, pneumonia, and DKA (or any cause of acidosis really).
Never forget to look for air under the diaphragm on a chest Xray.
Fluids
JVP, despite being the love child of all physicians and lecturers, has proven to be pretty unreliable when people have bothered to study it. Don’t rely on the JVP. Mucous membranes are similarly not great. Nor axillary moisture. Nor most of the things we are taught. Turns out fluid assessment is actually harder than they would have you believe. History is important- if I’ve been nauseated for 2 days I’m unlikely to keep up my fluid intake. The presence of thirst can be a good indicator (however remember that the elderly patient has decreased thirst response). If someone tells you ‘boy I’ve really been peeing since you hooked up that IV fluid’, they probably don’t need it. Urea can be a good indicator of dehydration as it can go up while Cr remains normal. I guess the message is form on overall clinical impression rather than relying on isolated and antiquated examination manoeuvres.
Normal saline should be called abnormal saline. It contains way too much chloride than the body can handle and when used for fluid resuscitation can cause an acidosis (as opposed to plasmalyte or lactated ringers which keeps the pH normal). The chloride load also shuts down renal blood flow. Both saline and plasmalyte contain way too much sodium than the body knows what to do with so should not be used for maintenance fluid (assuming your sodium is normal to begin with).
The first thing people think of when faced with hyponatremia is SIADH. This is however quite rare. Decide if the patient is euvolemic, hypovolemic or hypervolemic (easier said than done). If you are diagnosing SIADH frequently I can assure you you are doing something wrong. Remember you cannot interpret a high urine sodium in the context of diuretic use.
Correcting sodium is one of the examples of being able to take a largely healthy person and swiftly kill them with good intentions. IVF if given should be given slowly- the recommended rate is 1ml/kg/hr. Even better, if there is nothing stopping them from doing so, rehydrate orally. Learn your institutions recommendations for rate of Na correction. Check the Na q 2hours initially.
A 1.5 litre fluid restrict is not a fluid restrict.
The practice of pumping septic patients with fluid until they become breathless is dangerous. There are several recent studies to suggest that septic patients who receive more fluid do worse, accounting for baseline severity. Generally people with sepsis are not volume deplete, or dry, or whatever terms you wish to use. They are vasodilated and leaking fluid into their tissues. Within a few hours most of that bolus you have given will be in the tissues. Fluid should be given in measured aliquots in an attempt to improve hemodynamics and frequent reassessment made. If there is no response senior involvement should be sought early. Unfortunately many of your registrars will have been taught to “fill the tank” so this may not achieve much. But at least the buck has been moved up the line.
Urine output should not be chased like a kid after a Mr Whippy’s. It is simply a piece of the puzzle. Urine output, while affected by renal blood flow, is not indicative of renal blood flow. Many hormones influence how much water and sodium is reabsorbed in the tubules, many of which are secreted in acute illness. Trying to aggressively normalise the urine output in a septic patient, whose oliguria is due to a complex pathophysiology, will likely leave you recalling the next tidbit.
Mentioned above but bears repeating, in your first 6 months you will likely iatrogenically overload someone.
Fluids are a drug and should be viewed as such. They can cause significant harm.
Sugars
Peoples sugars go off when they are unwell. While hyperglycaemia is associated with complication rates postoperatively studies of tight glucose control have failed to show a benefit. Hypoglycaemia is more of a worry.
If the sugars are really haywire during acute unwellness better to put them on a GIK rather than adjust the regular insulin as eventually the insulin requirements will return to normal.
Learn the onset and duration of action of different insulins. Giving a repeat dose of novorapid because the sugar is still high after 45 minutes can lead you into great trouble.
Fever
The first thought for any febrile patient is sepsis, then sepsis, then sepsis. Thoughts are not equal to actions however, so this initial thought should be tempered by your clinical findings.
Blindly culturing all patients with fever is likely to lead to treatment of your own skin flora.
If you do think cultures are necessary then they don’t need to be timed with the fever- yield is identical whether taken at the time of the temperature or not.
A positive urine without urinary symptoms is unlikely to be an explanation for a fever. The diagnosis of UTI requires the presence of symptoms and simple bladder infections don’t really cause fever. The exception is people who are unable to give a history of urinary symptoms, where the diagnosis of UTI is really one of exclusion. This is all assuming they are not septic of course. Always be sceptical of a positive urine as a cause of anything.
Old people have high rates of urinary colonisation and pyuria. This does not mean they have a UTI unless there are other features of infection. People with catheters are universally colonised, so don’t culture the catheter unless you’ve already decided you’re going treat something.
Drugs cause fevers too.
Always look at the sacrum. Always looks at IV lines.
Neurology
A normal gait and pronator drift test make unilateral limb weakness unlikely.
Nobody can elicit the ankle jerk.
Any reflex worth eliciting can be elicited with the end of your stethoscope.
Raised ICP can produce deep t wave inversions on the ECG.
A Cushing reflex spells impending doom.
Don’t be alarmed by a blood pressure of 220/120 in your ischemic stroke patient. More importantly don’t try to lower it.
Learn the HINTS exam. Posterior strokes are easily missed and it is easy to gloss over this portion of the exam sometimes.
The last time I examined CNs VIII – XI was in medical school.
Drugs
Never ever sedate a patient with IV medication unless you know what you are doing (most likely you don’t)
Despite diazepam having a long half-life it has a much shorter duration of action than other benzos due to its lipid solubility. Read about the three compartment model (or whatever its called).
Naloxone should work straight away. If it doesn’t, look elsewhere.
Always check the QTc before giving haloperidol. A pain but worth it.
All antiemetics have the unfortunate side effect of prolonging your QT. In isolation not a problem but can be when they are combined with other QT prolonging drugs.
Haloperidol and dexamethasone are great antiemetics.
Digoxin is a real pain in the butt. If the renal function goes off, always check a level. Or If a patient on it complains of some non-specific, not otherwise explainable symptom. Especially visual disturbance.
Slow release metoprolol can be dissolved in water (but not crushed!)
An infuriating amount of people on frusemide don’t actually have heart failure. Treating venous stasis by dehydrating someone is like fixing a squeaky door by removing the door.
Blood pressure
The only reason to lower someone’s blood pressure acutely is if they have signs of end organ damage, and in this case this is done in an ICU setting. An otherwise well blood pressure of 200/100 does not need acute lowering and there is no place for stat doses of felodipine, etc.
It takes a little while for a dose change of antihypertensives to translate into a reduction of blood pressure. If you have increased someones antihypertensive and two days later their blood pressure is still high, this does not warrant increasing it further after a mere 2 days.
Hypotension is usually accompanied by tachycardia- unless the person is on B Blocking medication or has conduction disease. Opiates can also cause hypotension with normal heart rate through their sympathetic blocking mechanisms (especially epidurals!)
MAP is a more important indicator of organ perfusion than systolic/diastolic.
Fluid is unlikely to fix hypotension caused by vasoplegia. If you suspect hypotension caused by opiates, and you think treatment is necessary, better to stop the epidural or give a ‘baby’ dose of naloxone.
Blood pressure goes down when you are asleep.
The elderly
Taking a history from a demented/delirious patient is quite fruitless.
Asking a demented patient whether they have pain just won’t cut the mustard. Most hemiarthoplasty folks will say no. Then you gently move their hip and they jump off the bed.
In a similar vein untreated pain is a major cause of delirium/agitation.
While it requires no intellectual effort to send off a “delirium screen”, whatever that is, unfortunately most delirium is only reversible by the patient leaving the hospital and going back to their own familiar environment.
Dehydration is also an important cause of delirium- demented people don’t ask for water.
Never underestimate the therapeutic effect of working bowels.
Unfortunately because of all of the above, and doctors who don’t grasp the concept of dementia (or just want to finish their ward round), you will find that demented folks have their pain, bowels and hydration undertreated.
People can walk on hip fractures. Not well, but they can. Don’t be reassured that there is no fracture by the fact that the person is mobilising.
Xrays can miss fractures. Your clinical suspicion is important and don’t doubt yourself if things don’t quite add up.
General
A question asked in the history is only valuable if you know its significance and the patient doesn’t. This is why the chest pain history is so unrevealing- every man and their dog knows what heart pain is ‘supposed’ to sound like.
A perusal through past clinic letters can save you reinventing the wheel. Very simple but no-one ever seems to do it. Will make you look like you know heaps about your patients too.
Not every value needs to be ‘normalised’.
Never order a test if you don’t know what to do with the answer. I’m looking at you phosphate.
You will often get paged about things that are plain irritating. No matter how frustrated or stressed you are, always maintain a professional and calm manner with nurses. If people respect you, they also trust you.
When writing a discharge summary remember that the GP doesn’t care what the patients JVP was on admission. They do however want to know what the team thought was wrong, and what the ongoing plan is.
Always trust a parent when they say their child isn’t right.
The same cannot be said of a parent’s children. The statement ‘Mums cognition is usually fine’ should be viewed with some suspicion if said relative lives 45km away.
The patient who looks genuinely disappointed that you couldn’t find anything wrong with them has roughly a 105% chance of readmission.
Always doubt your diagnosis.
When teams read your on call note they will skip straight to the impression. Make it good. 1 line is not an impression. An impression should always include a working diagnosis, even if you are not sure, and alternatives should be noted with brief comments as to why or why not they are likely.
If you don’t pull out straight away, you will eventually hit a wiggly vein.
Each tidbit should be viewed as a starting point to look things up further rather than a direct recommendation.
Mostly these tidbits are backed up by relevant literature, however it is too tiresome to reproduce this below. If you have a burning desire you can PM me and I will see if I can find the references.
I have grouped them into hopefully sensible headings. Not alphabetical unfortunately.
Feel free to reply and add your own.
The heart
The patient on the ward who develops central chest pain has to be pretty exceptional to not warrant a troponin.
Learn about the STEMI equivalents. These are ECG findings that do not have ST elevation but require emergent PCI nonetheless. Hyperacute T waves and de Winters waves are two such examples. Wellens waves while not necessarily needing emergent PCI do signify a high risk of progressing to an anterior infarction.
In the vein of the above ischemic ST depression is diffuse. Localised ST depression should be viewed as reciprocal to ST elevation elsewhere until proven otherwise. If there is localised inferior depression, look at the lateral leads- a high lateral STEMI can present with only STE in aVL. Similarly ST depression in V2-4 is a posterior STEMI until proven otherwise- do posterior ECGs.
Diffuse ST depression with ST elevation in AVR can be a portender of left main occlusion and always warrants showing a medical registrar (or cardiology if there’s one around!)
T wave inversion is a sign of reperfusion not active ischemia. Flat t-waves, while often ignored, carry the same significance as t wave inversion.
Contrary to popular belief you can diagnose ischemia in a LBBB. Look up the Scarbossi criteria.
People can have ischemic chest pain that does not produce a troponin rise. However if someone has ischemia lasting several hours then this should produce a troponin rise.
Pain radiating to the right arm has proven to be more specific for an MI than pain radiating to the left arm.
What the patient tells you about this pain being similar or dissimilar from their previous MI is largely irrelevant. One study showed “pain similar to previous MI” was actually a predictor of non-ischemic chest pain.
People without obstructive CAD can still have MIs- plaque of any size is capable of rupturing.
Intracranial pathology can produce ischemic ECG changes and troponin rises- always discuss with a senior first in someone who has had an intracranial event before starting ACS treatment.
Heart failure can be subtle and does not necessarily present with overt crackles and edema. If in doubt a BNP is useful – if it is negative. BNP is sensitive but not specific.
Be cautious with frusemide- it is easier to give more than undo the kidney injury you have caused. 5mg IV may produce significant diuresis in a frusemide naïve patient, while in someone with significant CKD, 40mg may barely touch them. It is not good enough to give the frusy then walk away. They should become polyuric in the next few hours and if not, the dose isn’t enough.
It is really easy to iatrogenically overload patients and the likelihood is high you will do it within your first 6 months.
I am yet to meet heart sounds that weren’t dual. This is true even in the BMI 65 patient who leaves you tapping the diaphragm of your stethoscope in a perplexed manner. I have concluded that people are simply too embarrassed to document that they couldn’t hear the heart.
For some reason there is high frequency of coronary events at night (a literature proven phenomenon). Something to do with sympathetic surges during REM sleep.
Lungs
An ABG makes you feel like you are doing something useful but rarely adds a lot in the majority of instances it is done. If you ABG a desaturating patient you will find, surprise surprise, hypoxia. Except now you start to panic because a PO2 of 6.5 looks scarier than a saturation of 88%, but in reality they may be one and the same. You should always be looking for something specific on it, that you can’t get at the bedside, for example CO2. If you don’t care about the CO2 and only want the pH, bicarb etc. a venous gas will do the same job and is far less painful for the patient.
A normal respiratory rate in someone with respiratory distress is concerning rather than reassuring as it suggests they are about to tire.
You cannot make a chronic CO2 retainer stop breathing by giving oxygen. You can drive up their CO2 but this is dependent on the saturations i.e. exceeding 88-92, rather than the flow rate on the wall.
Learn to talk in FiO2 where it is measurable.
Asthmatics should have a respiratory alkalosis on their gas- a normal CO2 is concerning and a high CO2 is terrifying. Going off the above- terror is a legitimate reason for an immediate phone call to a senior.
A talking, alert, oriented patient is a lot less likely to be in acute CO2 retention.
Wheeze is not specific for COPD. Heart failure can give you wheeze. PE can give you wheeze. A lot of things can give you wheeze.
Similarly a COPD patient with an exacerbation may not necessarily have a wheeze until you improve their air entry. Don’t discount COPD based on the absence of a wheeze.
While you won’t be making changes to BiPAP, it is useful to know what IPAP and EPAP are and how they can be changed to affect oxygenation and ventilation.
Salbutamol causes a high lactate-which doesn’t need anything done about it.
PE doesn’t read the textbook. A lot of things don’t, but I feel this is especially true of PE. Don’t regard the Wells criteria as gospel.
You don’t develop an aspiration pneumonia straight away. You develop a chemical pneumonitis. The infection may or may not develop in several days.
What goes on in the abdomen affects respiratory mechanics almost as much as what goes in the chest.
Abdomen/surgery
A lot of examination manoeuvres are taught in depth but generally useless. The abdomen is poorly taught but very very useful. Feel a lot of abdomens in medical school. Train yourself to look closely for scars every time you looks at the abdomen (oh yes I forgot I had my spleen out in 1969).
Normal bloods reduce the likelihood of appendicitis, diverticulitis, etc. They don’t rule them out however. Neither does lack of a fever. This is especially true at the extreme ends of age. A significant proportion of the elderly may have abdominal pathology but normal bloods.
I can count on one hand the number of spleens I have felt in my life.
Bulging flanks (a simple end of bend observation) is more sensitive for ascites than shifting dullness. Don’t believe the hype.
No matter how much radiology objects an ultrasound should always be sought before draining ascites. This becomes apparent when everybody, including the consultant, comments on the gross ascites only to discover that actually the patient is probably just really fat. Do you trust your own examination enough to go blindly sticking needles?
It turns out the adage that people with appendicitis don’t keep eating has been debunked several times. This won’t stop consultants from commenting that the patient probably doesn’t have appendicitis because he’s munching on KFC.
Fever within the first 1-2 days post op is common and if the patient is clinically well and examines normally does not need investigating.
Urine output is unreliable post op as the stress response to surgery causes an antidiuresis. Some sources suggest 0.2ml/kg/hour is normal. Don’t give fluid based solely on a urine output. Positive fluid balance is associated with increased risk of anastomotic breakdown etc.
In fact it seems the less you touch your patients postoperatively the better they do.
Always suspect ischemic bowel in someone in heaps of pain, but who is not very tender. A lactate is useful however a normal one is not necessarily reassuring. For some reason HD patient are at really high risk of ischemic bowel.
After acute bleeding the Hb may initially remain stable. It takes a few hours for the “autotransfusion” of fluid shifting from interstitial to vascular space, thereby diluting haemoglobin.
Don’t trust an Xray to tell you about constipation. Also it is normal to have feces in the colon on Xray- that is the purpose of the colon! If you’re doing an Xray to look for faecal loading you need to stop being lazy and do a rectal!
Don’t lie to the patient by telling them “this rectal won’t hurt”. Better to be honest.
Remember there are non-surgical causes of abdominal pain. Chief not to forget are MI, pneumonia, and DKA (or any cause of acidosis really).
Never forget to look for air under the diaphragm on a chest Xray.
Fluids
JVP, despite being the love child of all physicians and lecturers, has proven to be pretty unreliable when people have bothered to study it. Don’t rely on the JVP. Mucous membranes are similarly not great. Nor axillary moisture. Nor most of the things we are taught. Turns out fluid assessment is actually harder than they would have you believe. History is important- if I’ve been nauseated for 2 days I’m unlikely to keep up my fluid intake. The presence of thirst can be a good indicator (however remember that the elderly patient has decreased thirst response). If someone tells you ‘boy I’ve really been peeing since you hooked up that IV fluid’, they probably don’t need it. Urea can be a good indicator of dehydration as it can go up while Cr remains normal. I guess the message is form on overall clinical impression rather than relying on isolated and antiquated examination manoeuvres.
Normal saline should be called abnormal saline. It contains way too much chloride than the body can handle and when used for fluid resuscitation can cause an acidosis (as opposed to plasmalyte or lactated ringers which keeps the pH normal). The chloride load also shuts down renal blood flow. Both saline and plasmalyte contain way too much sodium than the body knows what to do with so should not be used for maintenance fluid (assuming your sodium is normal to begin with).
The first thing people think of when faced with hyponatremia is SIADH. This is however quite rare. Decide if the patient is euvolemic, hypovolemic or hypervolemic (easier said than done). If you are diagnosing SIADH frequently I can assure you you are doing something wrong. Remember you cannot interpret a high urine sodium in the context of diuretic use.
Correcting sodium is one of the examples of being able to take a largely healthy person and swiftly kill them with good intentions. IVF if given should be given slowly- the recommended rate is 1ml/kg/hr. Even better, if there is nothing stopping them from doing so, rehydrate orally. Learn your institutions recommendations for rate of Na correction. Check the Na q 2hours initially.
A 1.5 litre fluid restrict is not a fluid restrict.
The practice of pumping septic patients with fluid until they become breathless is dangerous. There are several recent studies to suggest that septic patients who receive more fluid do worse, accounting for baseline severity. Generally people with sepsis are not volume deplete, or dry, or whatever terms you wish to use. They are vasodilated and leaking fluid into their tissues. Within a few hours most of that bolus you have given will be in the tissues. Fluid should be given in measured aliquots in an attempt to improve hemodynamics and frequent reassessment made. If there is no response senior involvement should be sought early. Unfortunately many of your registrars will have been taught to “fill the tank” so this may not achieve much. But at least the buck has been moved up the line.
Urine output should not be chased like a kid after a Mr Whippy’s. It is simply a piece of the puzzle. Urine output, while affected by renal blood flow, is not indicative of renal blood flow. Many hormones influence how much water and sodium is reabsorbed in the tubules, many of which are secreted in acute illness. Trying to aggressively normalise the urine output in a septic patient, whose oliguria is due to a complex pathophysiology, will likely leave you recalling the next tidbit.
Mentioned above but bears repeating, in your first 6 months you will likely iatrogenically overload someone.
Fluids are a drug and should be viewed as such. They can cause significant harm.
Sugars
Peoples sugars go off when they are unwell. While hyperglycaemia is associated with complication rates postoperatively studies of tight glucose control have failed to show a benefit. Hypoglycaemia is more of a worry.
If the sugars are really haywire during acute unwellness better to put them on a GIK rather than adjust the regular insulin as eventually the insulin requirements will return to normal.
Learn the onset and duration of action of different insulins. Giving a repeat dose of novorapid because the sugar is still high after 45 minutes can lead you into great trouble.
Fever
The first thought for any febrile patient is sepsis, then sepsis, then sepsis. Thoughts are not equal to actions however, so this initial thought should be tempered by your clinical findings.
Blindly culturing all patients with fever is likely to lead to treatment of your own skin flora.
If you do think cultures are necessary then they don’t need to be timed with the fever- yield is identical whether taken at the time of the temperature or not.
A positive urine without urinary symptoms is unlikely to be an explanation for a fever. The diagnosis of UTI requires the presence of symptoms and simple bladder infections don’t really cause fever. The exception is people who are unable to give a history of urinary symptoms, where the diagnosis of UTI is really one of exclusion. This is all assuming they are not septic of course. Always be sceptical of a positive urine as a cause of anything.
Old people have high rates of urinary colonisation and pyuria. This does not mean they have a UTI unless there are other features of infection. People with catheters are universally colonised, so don’t culture the catheter unless you’ve already decided you’re going treat something.
Drugs cause fevers too.
Always look at the sacrum. Always looks at IV lines.
Neurology
A normal gait and pronator drift test make unilateral limb weakness unlikely.
Nobody can elicit the ankle jerk.
Any reflex worth eliciting can be elicited with the end of your stethoscope.
Raised ICP can produce deep t wave inversions on the ECG.
A Cushing reflex spells impending doom.
Don’t be alarmed by a blood pressure of 220/120 in your ischemic stroke patient. More importantly don’t try to lower it.
Learn the HINTS exam. Posterior strokes are easily missed and it is easy to gloss over this portion of the exam sometimes.
The last time I examined CNs VIII – XI was in medical school.
Drugs
Never ever sedate a patient with IV medication unless you know what you are doing (most likely you don’t)
Despite diazepam having a long half-life it has a much shorter duration of action than other benzos due to its lipid solubility. Read about the three compartment model (or whatever its called).
Naloxone should work straight away. If it doesn’t, look elsewhere.
Always check the QTc before giving haloperidol. A pain but worth it.
All antiemetics have the unfortunate side effect of prolonging your QT. In isolation not a problem but can be when they are combined with other QT prolonging drugs.
Haloperidol and dexamethasone are great antiemetics.
Digoxin is a real pain in the butt. If the renal function goes off, always check a level. Or If a patient on it complains of some non-specific, not otherwise explainable symptom. Especially visual disturbance.
Slow release metoprolol can be dissolved in water (but not crushed!)
An infuriating amount of people on frusemide don’t actually have heart failure. Treating venous stasis by dehydrating someone is like fixing a squeaky door by removing the door.
Blood pressure
The only reason to lower someone’s blood pressure acutely is if they have signs of end organ damage, and in this case this is done in an ICU setting. An otherwise well blood pressure of 200/100 does not need acute lowering and there is no place for stat doses of felodipine, etc.
It takes a little while for a dose change of antihypertensives to translate into a reduction of blood pressure. If you have increased someones antihypertensive and two days later their blood pressure is still high, this does not warrant increasing it further after a mere 2 days.
Hypotension is usually accompanied by tachycardia- unless the person is on B Blocking medication or has conduction disease. Opiates can also cause hypotension with normal heart rate through their sympathetic blocking mechanisms (especially epidurals!)
MAP is a more important indicator of organ perfusion than systolic/diastolic.
Fluid is unlikely to fix hypotension caused by vasoplegia. If you suspect hypotension caused by opiates, and you think treatment is necessary, better to stop the epidural or give a ‘baby’ dose of naloxone.
Blood pressure goes down when you are asleep.
The elderly
Taking a history from a demented/delirious patient is quite fruitless.
Asking a demented patient whether they have pain just won’t cut the mustard. Most hemiarthoplasty folks will say no. Then you gently move their hip and they jump off the bed.
In a similar vein untreated pain is a major cause of delirium/agitation.
While it requires no intellectual effort to send off a “delirium screen”, whatever that is, unfortunately most delirium is only reversible by the patient leaving the hospital and going back to their own familiar environment.
Dehydration is also an important cause of delirium- demented people don’t ask for water.
Never underestimate the therapeutic effect of working bowels.
Unfortunately because of all of the above, and doctors who don’t grasp the concept of dementia (or just want to finish their ward round), you will find that demented folks have their pain, bowels and hydration undertreated.
People can walk on hip fractures. Not well, but they can. Don’t be reassured that there is no fracture by the fact that the person is mobilising.
Xrays can miss fractures. Your clinical suspicion is important and don’t doubt yourself if things don’t quite add up.
General
A question asked in the history is only valuable if you know its significance and the patient doesn’t. This is why the chest pain history is so unrevealing- every man and their dog knows what heart pain is ‘supposed’ to sound like.
A perusal through past clinic letters can save you reinventing the wheel. Very simple but no-one ever seems to do it. Will make you look like you know heaps about your patients too.
Not every value needs to be ‘normalised’.
Never order a test if you don’t know what to do with the answer. I’m looking at you phosphate.
You will often get paged about things that are plain irritating. No matter how frustrated or stressed you are, always maintain a professional and calm manner with nurses. If people respect you, they also trust you.
When writing a discharge summary remember that the GP doesn’t care what the patients JVP was on admission. They do however want to know what the team thought was wrong, and what the ongoing plan is.
Always trust a parent when they say their child isn’t right.
The same cannot be said of a parent’s children. The statement ‘Mums cognition is usually fine’ should be viewed with some suspicion if said relative lives 45km away.
The patient who looks genuinely disappointed that you couldn’t find anything wrong with them has roughly a 105% chance of readmission.
Always doubt your diagnosis.
When teams read your on call note they will skip straight to the impression. Make it good. 1 line is not an impression. An impression should always include a working diagnosis, even if you are not sure, and alternatives should be noted with brief comments as to why or why not they are likely.
If you don’t pull out straight away, you will eventually hit a wiggly vein.
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