Pancreatitis - we use the 2/3 critieria. Typically symptoms, constant abdo pain radiating to the back, lipase 3 x normal limit and imaging of the pancreas to show inflammation. If we have typical symptoms with an elevated lipase, we may not need a CT of the pancreas (refer to Balthazar classification).
Like most internal medicine things we go through are causes such as infections, malignancies, genetic, autoimmune, etc.
1. drugs - azathioprine, steroids, valproic acid, thiazide
2. infections (though low yield but associated with viruses like mumps)
3. etoh
4. gallstones
5. familial
6. trauma
7. Sphinctor of oddi dysfunction
Most commonly - alcohol and gallstones. Everyone needs an abod ultrasound to rule out gallstones, hwoever, ALT 3 x normal limit has a positive predictive value of 95% so woudl consider US right away if they were jaundice, feverish with RUQ pain to suggest ascending cholangitis from a blocked stone which would give them a ticket for ERCP to get that stone out!
Remember - patients deemed "idiopathic" most often have biliary sludge or microlithiasis, this can be found by ERCP. Potentially an MRCP or endoscopic ultrasound can be used to look for tumors/cancer in individuals with B symptoms or elderly.
We have multiple scoring systems to predict mortality, choose one!
BISAP, APACHE 2, and the classic Ransons.
Bisap is quite easy, but it does incorporate you knowing SIRS criteria (needed 2/4).
Complications range from acute to chronic.
Acute
I mentioned ARDS in class, they also get atelectasis, and pleural effusions. As they secrete enzymes from the pancreas when it is inflamed, one theory for atelectasis is the release of phospholipase A2 which breaks down phospholipids, which make up a large portion of surfactant! NO surfactant? airways have trouble staying open!
The pleural effusion is usually left sided and is because a pancreatic-pleural fistula can form. If patients are febrile 48 hours after, consider abscess, CT and general surgery consult or IR to drain it.
Chronic
Splenic vein thrombosis is possible because this vein sits behind the pancreas, making it vulnerable. We are careful to anticoagulate these clots because of concerns of hemorrhage in an inflamed pancreas. Pseodocysts are the feared complication patients get AFTER their pancreatitis has resolved, with increasing abod pain, these are generally drained when not resolving after 6 weeks (classically) or >6 cm. They can be drained by GI or IR, often going through the stomach! Pancreatic insufficiency can result in diabetes, as well us vitamin deficiencies ADEK, we treat this with pancreatic enzymes. They can have chronic abdo pain, fat in stools (grey stools) and calcifcation seen on abdo xray.
So how do we treat pancreatitis? Often a conservative approach, manage pain with opioids, NG tube for an ileus, and we NOW know feeding earlier is better. Studies comparing NG vs NJ having shown vast differences, but ideally and NJ tube for someone who has pain or does not want to eat at 48-72 hrs is ideal because we would be bypassing the pancreas. We know feeding patients enterally compared to TPN has mortality benefit, this thought of providing GUT nutrition.
Finally, there are other causes of elevated lipase - DKA often it can elevated (mechanism not completely clear), perforated peptic ulcer, ischemic gut, HIV, renal failure. Need to look for classic symptoms!
Saturday, 28 March 2015
Differential-icious Pancytopenia March 25th
The differential for pancytopenia is enormous, 100s of case reports on finding everything associated with pancytopenia. Like any cell like that is look, we generally consider decrease production, increase destruction (or sequestration). Blood loss is more specific to red blood cells
A general approach
Pancytopenia
PNH – complement mediated red cell lysis
Aplastic anemia
-
idiopathic
-
- infections (EBV, cmv, heb c, HIV)
-
drug induced (chemo, methotrexate,
anti-epileptics)
-
toxins – alcohol
neoplastic – leukemia (AML, CLL), MDS, bone marrow mets
infections – sepsis, TB, histo leishmaniasis
insufficiency – folate, B12, copper
iatrogenic – chemotherapy
consumption – hyperspelnism, immune-mediated (lupus,
scleroderma)
Inherited – HLH, (acquired is macrophage activation
syndrome)) increase triglycerides, low fibrinogen, high ferritin, liver enzyems
So how do you approach the patient? As always a history and physical may be revealing. B symptoms may suggest malignancy, history of cancer may suggest metastasis to the bone. Neurological findings can suggest b12 deficiency. Consider infectious causes such as hepatitis if risk factors (IVDU), HIV risk factors (male male intercourse). ANY new medications need to be considered as many MANY medications have been associated with pancytopenia.
In terms of investigations, fortunately we can look to reticulocyte count (which after a CBC and peripheral smear... should be our FIRST step) to see if this is a bone marrow production problem.
If the reticu count is high (appropriately responding) we need to consider blood loss + sequestration, destruction etc. **note unfortunately we do not test for a reticulocyte equivalent for platelets and wbcs.
We may look to MCV for some tips (mainly for very high MCV we consider b12/folate deficiency).
Ultimately, bone marrow is the gold standard in helping us make a diagnosis. Specifically it rules out scary things such as leukemia which would need to be treated ASAP.
We briefly discussed how blood malignancies can produce pancytopenia - bone marrow is compact with cells, nothings gets out! Generally we would hope we could some immature (blast) cells to tip us off that it is leukemia.
Aplastic anemia typically shows fat cells, and gives us a dry tap.
b12 deficiency (which we believe is the cause of OUR patients pancytopenia) is needed to make all cell lines, its used to TAKE OFF methyl groups off of tetrahydrofolate (THF) so that other carbon groups can be added on to make DNA molecules. We could assess this with a b12 level, but the assay isn't the greatest and b12 deficient individuals can be found with levels that are normalish. Generally levels 100-300 make us concerned for b12 deficiency, and thus we would send off a methylmalonic acid (and a homocysteine level as well).
Often people would just empirically give vit b12.
What causes b12 deficiency - many things! pernicious anemia, tea and toast diet, pancreatic insufficiency, crohn's disease, gastric bypass. Why is the cause important? If it were a malabsorption issue, we would want to give IM injections every month as opposed to oral pills daily.
In terms of investigations, fortunately we can look to reticulocyte count (which after a CBC and peripheral smear... should be our FIRST step) to see if this is a bone marrow production problem.
If the reticu count is high (appropriately responding) we need to consider blood loss + sequestration, destruction etc. **note unfortunately we do not test for a reticulocyte equivalent for platelets and wbcs.
We may look to MCV for some tips (mainly for very high MCV we consider b12/folate deficiency).
Ultimately, bone marrow is the gold standard in helping us make a diagnosis. Specifically it rules out scary things such as leukemia which would need to be treated ASAP.
We briefly discussed how blood malignancies can produce pancytopenia - bone marrow is compact with cells, nothings gets out! Generally we would hope we could some immature (blast) cells to tip us off that it is leukemia.
Aplastic anemia typically shows fat cells, and gives us a dry tap.
b12 deficiency (which we believe is the cause of OUR patients pancytopenia) is needed to make all cell lines, its used to TAKE OFF methyl groups off of tetrahydrofolate (THF) so that other carbon groups can be added on to make DNA molecules. We could assess this with a b12 level, but the assay isn't the greatest and b12 deficient individuals can be found with levels that are normalish. Generally levels 100-300 make us concerned for b12 deficiency, and thus we would send off a methylmalonic acid (and a homocysteine level as well).
Often people would just empirically give vit b12.
What causes b12 deficiency - many things! pernicious anemia, tea and toast diet, pancreatic insufficiency, crohn's disease, gastric bypass. Why is the cause important? If it were a malabsorption issue, we would want to give IM injections every month as opposed to oral pills daily.
March 23rd, hyponatremia
Hyponatremia – common issue of hospitalized patients. We have limited amount of evidence for treating hyponatremia, specifically a lack of RCTs. Searching through the literature there are review
articles and case reports/series. If you have the time
Like always, we assess for stability, someone who is
hyponatremia and seizing we’d consider given them a bolus of 3% normal saline
of 150 mL over 20 minutes (as per europena guidelines, uptodate suggest 100 mL of 3% bolus. Knowing that there is an increased risk of osmotic demyelination (which was originally
described in severely malnourished alcoholics).
Once they are stable, we consider acute vs chronic
hyponatremia, acute changes can generally be changed more quickly because the
brain has not had time to adjust its osmolality (a low number).
More often than not we don’t know the acuity, so correcting
it slowly is best.
Next we need an approach – easiest thing is to first rule
out pseudohyponatremia, lipids, protein and glucose. Often books will discuss
how glucose is a true cause and this is because the excessive glucose will pull
water into the intravascular space. In
DKA we add 3 to the sodium for every 10 glucose above 10 because once we lower
glucose, water will dissipate and thus THAT will be the left over value.
Multiple myeloma with excessive protein is a classic
pseduohyponatremia – extra points on your future rotations if you know that an
arterial blood gas can be used to find a TRUE sodium, important because a
pseudo and true hyponatremia can be present at the same time. MM may also present with a normal anion gap!
So you check the serum osm and it comes back at 240, so this
is true hyponatremia! Next step is usually to look at the volume status.
I start with the overloaded patient – on exam, pitting
edema, increased jVP, ascites (S3 heart sound if you believe you can hear
it!). It is due to three things: CHF, liver cirrhosis, and nephrotic syndrome –
all of these patients will have elevated ADH levels related to the kidney
thinking its underperfused… high ADH levels means reabsorption of water and diluting serum sodium.
Urine sodium in the above situations is usually on the lower side because of decreased effective circulating volume and thus aldosterone levels are high which will reabsorb sodium.
Urine sodium in the above situations is usually on the lower side because of decreased effective circulating volume and thus aldosterone levels are high which will reabsorb sodium.
In all of the above, specifically CHF and cirrhosis, the low
sodium usually is a poor prognostic sign, refer to MELD sodium and (http://www.ncbi.nlm.nih.gov/pubmed/15719386), however if serum sodium is less than 120, consider another mechanism
(sig. increase free water, new medication, etc.)
Hypovolemic is next consideration because its easier. The
classic situation is someone with vomiting or diarrhea (getting rid of isotonic
fluids) and ingestion free water to stay
hydrated.
On exam: we look for tachycardia, hypotension, orthostatic
vital signs (change in HR 30, SBP 20, and DBP 10), dry axilla, dry mucous membranes.
Other causes are burn victims, blood loss (all with increase
free water intake). In this situation urine osm should be high and urine sodium
should be low – they are concentrating their urine and reabsorption sodium so
water can follow
Pearl: adrenal insufficiency causing hypotension/dehydrated
state with an increased urine sodium because aldosterone levels are low.
FYI – free water doesn’t mean they stole it, or it was given
to them , it refers to water without solute.
Another situation is after marathons, taking lots of water
in. The concern with DROPPING sodium so quickly is cerebral edema.
Finally and most commonly seen issue in my practice is the euvolemic hyponatremia, though often it can be difficult to tease out if its euvolemic or mildly hypovolemic.
If the urine osm is less than 100, it essentially tells they have psychogenic polydipsia with decrease solute intake.
Euvolemic hypotonic hyponatremia
SIADH: (increase urine osm, normal urine sodium, decrease BUN)
- malignancy, lung, brain, GI, lymphoma
- pulmonary - pneumonia, asthma, copd
- intracranial: trauma, stroke, hemorrhage
- drugs: SSRIs probably the most responsible, antipsychotics, anti-epileptics, MDMA
- other: pain, nausea, post op!
Endocrine: increase ADH is seen with decrease glucorcoticoid (adrenal insuff), also hypothyroid
psychogenic polydipsia: usually drinking >12 L/day of water, urine osm <100, often associated with very low uric acid levels
*from pocket medicine
Low solute: "tea and toaste" beer potomania" - decrease daily solute load, increase free water, insufficient solute to excrete water intake (if only 250 mOsm/day, minimum urine Osm = 60 mOsm/L - excrete in ~4 L; if water ingestion exceeds this, we have water retention).
If symptomatic aka seizure acute decrease LOC, 3% NS 150 mL over 20 min is ideal with repeating lights stat immediately after.
If hypovolemic - treat with NS, give slowly ~75 mL/hr frequent checking of lytes (there is a formula to calculate this).
SIADH - free water restrict, can consider salt tabs if chronic and no CHF, fix underlying cause
hypervolemic - mobilize fluid intravascularly, lasix for CHF, consider albumin in cirrhotics, consider
Fluid restriction, ~1.5 L/day.“vaptans” are a class of medication that exists but in RCTs
give a mild benefit over fluid restriction and are very expensive.
Below is one of the many charts that gives a breakdown, never hurts to have a look before diagnosing a cause of hyponatremia in patients.
Saturday, 21 March 2015
March 18th, Stroke
Quick mention on stroke
Consider other causes if decreased LOC, hypoglycemic? low BP? seizure?
Remember FAST exam, facial droop, arm weakness/drift, speech slurring/ timing (4.5 hours!)
First test - CT head without contrast, looking for a bleed - if present... can't give TPA
Neurology should be called ASAP, we will often perform NIH stroke scale score, if scores are too low we may not give as we know they have little gain but still have a chance to bleed. If scores are very high, they also may be at risk of hemorrhagic conversion.
6% of patients given TPA as per initial NINDS trial. From this original trial there was no mortality benefit but better outcomes in regards to morbidity.
Before TPA, must go through checklist as similar to PE to check for contraindications.
So you've decided they can't get TPA, but they've had a stroke... what's next?
If a large MCA, "malignant MCA" - with edema, call neurosurg as they may benefit from a hemicraniectomy.
Now we consider causes of the stroke, most commonly afib, ECG, HTN, artery-artery, and when nothing comes up.. consider stranger things like vasculitis or paradoxical emboli.
Things to order MRI/MRA - looking for plaque in carotids (benefit from endarterectomy if done within 2 weeks)
Echo - looking for thrombus, calcification on valves, apical hypokinesis as a cause of the stroke
ECG - afib
HbA1c, lipid profile
Start high dose statin as per the SPARCL trial (although individuals had LDL >2).
If a large stroke and afib- might just start aspirin, repeat Ct head in 24 and 48 hours to ensure no bleeding.
If the cause is thought to be related to atherosclerosis, may consider aspirin and plavix for 3 weeks and then plavix after as per the CHANCE trial, which was studied in asian patients, slightly younger age.
Neurologists may have their own opinion about what to do in specific situations.
Refer to stroke rehab!
Also - blood pressure, we let them permissively go high (upto around 220) as to increase cerebral perfusion for ~3-5 dys.
Consider other causes if decreased LOC, hypoglycemic? low BP? seizure?
Remember FAST exam, facial droop, arm weakness/drift, speech slurring/ timing (4.5 hours!)
First test - CT head without contrast, looking for a bleed - if present... can't give TPA
Neurology should be called ASAP, we will often perform NIH stroke scale score, if scores are too low we may not give as we know they have little gain but still have a chance to bleed. If scores are very high, they also may be at risk of hemorrhagic conversion.
6% of patients given TPA as per initial NINDS trial. From this original trial there was no mortality benefit but better outcomes in regards to morbidity.
Before TPA, must go through checklist as similar to PE to check for contraindications.
So you've decided they can't get TPA, but they've had a stroke... what's next?
If a large MCA, "malignant MCA" - with edema, call neurosurg as they may benefit from a hemicraniectomy.
Now we consider causes of the stroke, most commonly afib, ECG, HTN, artery-artery, and when nothing comes up.. consider stranger things like vasculitis or paradoxical emboli.
Things to order MRI/MRA - looking for plaque in carotids (benefit from endarterectomy if done within 2 weeks)
Echo - looking for thrombus, calcification on valves, apical hypokinesis as a cause of the stroke
ECG - afib
HbA1c, lipid profile
Start high dose statin as per the SPARCL trial (although individuals had LDL >2).
If a large stroke and afib- might just start aspirin, repeat Ct head in 24 and 48 hours to ensure no bleeding.
If the cause is thought to be related to atherosclerosis, may consider aspirin and plavix for 3 weeks and then plavix after as per the CHANCE trial, which was studied in asian patients, slightly younger age.
Neurologists may have their own opinion about what to do in specific situations.
Refer to stroke rehab!
Also - blood pressure, we let them permissively go high (upto around 220) as to increase cerebral perfusion for ~3-5 dys.
March 17th, Treating PE
We spent a separate morning report on treating PE.
We know that ~50% of PE can be treated as an outpatient, refer to the OTPE trial, they classified patients with pulmonary embolism severity index (low and high risk), had patients randomized to outpatient vs inpatient treatment and demonstrated noninferiority.
In the index we specifically look for things like vital sign stability and patients not requiring oxygen.
So what do we use to treat them? First we consider idiopathic vs a cause of PE. With a suspected cause, we generally treat for 3 months (then reassess) and often stop. If idiopathic, we often repeat a D-dimer, if elevated treatment is prolonged. If low, we know there is significantly lower chance of recurrance (refer to PROLONG trial).
The one concerning feature of "idiopathic" PE is that they can be associated with malignancies, especially in the elderly. Basic screening should be assessed (mammogram in woman, colonoscopy, prostate cancer and a good physical exam and history of B symptoms).
Individuals with malignancy related PE have less recurrence when treated with LMWH compared to warfarin (refer to CLOT trial), in this study most patients had solid tumors, dose is 200 Units/kg. We have no available evidence for the New Oral Anticoagulants (NOACs).
When can you use a NOAC, in many patients dabigatran and rivaroxaban are ideal. Apixaban has been studied but is not approved in Canada yet.
Apixaban is ok in individuals with a GFR <25, they will take 15 mg BID x 3 weeks then 20 mg po daily (the afib dose also). The thing to watch out for... there is no clear reversible agent.
If someone has fluctuating creatinine one may consider IV heparin it is not effective much by kidney function. It's short half life also makes it ideal in patients who may bleed, in addition, there is a reversible agent (protamine sulfate).
Finally, what about submassive PE.
Massive is right heart strain (by echo, CT, RBBB or trop increase) and bp <90
Submassive: right heart strain with ok bp ?90
although the PEITHO trial found a decrease in primary ends points (mortality and hemodynamic instability), these aren't quite the same... dying vs hemodynamic stability are NOT the same things.
The MOPETT trial in 2012 showed that low dose TPA (50 mg instead of 100, the same dose in pEITHO) reduced pulmonary artery pressures (RVSP) that was maintained at 28 months. So maybe we have a risk of bleed now... for a decrease chance of pulmonary HTN in the future.
So what do we do now? For patients with submassive, acute onset, age less than 60... one may consider it, but important to rule out contraindications for PE (hemorrhagic stroke, recent surgery, brain tumor, etc. go through the checklist).
We know that ~50% of PE can be treated as an outpatient, refer to the OTPE trial, they classified patients with pulmonary embolism severity index (low and high risk), had patients randomized to outpatient vs inpatient treatment and demonstrated noninferiority.
In the index we specifically look for things like vital sign stability and patients not requiring oxygen.
So what do we use to treat them? First we consider idiopathic vs a cause of PE. With a suspected cause, we generally treat for 3 months (then reassess) and often stop. If idiopathic, we often repeat a D-dimer, if elevated treatment is prolonged. If low, we know there is significantly lower chance of recurrance (refer to PROLONG trial).
The one concerning feature of "idiopathic" PE is that they can be associated with malignancies, especially in the elderly. Basic screening should be assessed (mammogram in woman, colonoscopy, prostate cancer and a good physical exam and history of B symptoms).
Individuals with malignancy related PE have less recurrence when treated with LMWH compared to warfarin (refer to CLOT trial), in this study most patients had solid tumors, dose is 200 Units/kg. We have no available evidence for the New Oral Anticoagulants (NOACs).
When can you use a NOAC, in many patients dabigatran and rivaroxaban are ideal. Apixaban has been studied but is not approved in Canada yet.
Apixaban is ok in individuals with a GFR <25, they will take 15 mg BID x 3 weeks then 20 mg po daily (the afib dose also). The thing to watch out for... there is no clear reversible agent.
If someone has fluctuating creatinine one may consider IV heparin it is not effective much by kidney function. It's short half life also makes it ideal in patients who may bleed, in addition, there is a reversible agent (protamine sulfate).
Finally, what about submassive PE.
Massive is right heart strain (by echo, CT, RBBB or trop increase) and bp <90
Submassive: right heart strain with ok bp ?90
although the PEITHO trial found a decrease in primary ends points (mortality and hemodynamic instability), these aren't quite the same... dying vs hemodynamic stability are NOT the same things.
The MOPETT trial in 2012 showed that low dose TPA (50 mg instead of 100, the same dose in pEITHO) reduced pulmonary artery pressures (RVSP) that was maintained at 28 months. So maybe we have a risk of bleed now... for a decrease chance of pulmonary HTN in the future.
So what do we do now? For patients with submassive, acute onset, age less than 60... one may consider it, but important to rule out contraindications for PE (hemorrhagic stroke, recent surgery, brain tumor, etc. go through the checklist).
March 16th, Pulmonary Embolus and shortness of breath
On Monday March 16th we discussed an interesting case of pulmonary embolus. We had a woman who presented with syncope, hypotension (that improved with fluids) and tachycardia.
As I was not aware of the syncopal episode, I gave an approach to shortness of breath :)
Basically, heart, lungs, low hemoglobin and anxiety are the causes of shortness of breath.
Heart:
a. endocardium (valvular disease - aortic stenosis, aortic regurg, mitral stenosis, MR)
b. conduction system issues,
1. bradycardia - sick sinus, AV blocks,
2. Tachycardias - a-fib, aflutter, AVNRT, also VTs
b. myocardium
1. systolic failure (secondary to CAD, etoh, HTN, viral causes)
2. Diastolic failure (HTN, AS, HOCM).
c. CAD - shortness of breath can be an angina equivalent, mechanism is ischemia stiffens the myocardium, increasing pressures in the pulm circulation.
d. pericardium - tamponade, constrictive pericarditis
Lungs:
1. Alveol:
a: pulmonary edema (HF, ARDS)
b: pneumonia
2. Airways
a. Suprathoracic - laryngeal edema, or tumor (generally normal oxygenation, STRIDOR - generally inspiratory high pitched sound)
b. Intrathoracic - asthma, COPD
3. Blood vessels
a. Pulmonary embolus
b. primary pulmonary hypertension
4. Pleural
a. pneumothorax
b. pleural effusions (transudative/exudative)
5. Interstitium
a. edema
b. inflammatory
1. Organic exposure (hay, cotton)
2. Mineral exposures (asbestos, silicosis, coal)
3. Idiopathic disease (sarcoid, lupus, slceroderms)
Anemia
When any adult patient comes into the emergency room with shortness of breath we always start with vital signs, ABCs and make sure they are stable. History, physical exam and then are starting point would be CXR, ECG, and hemoglobin (this are simple tests that can dramatically change management).
We discussed some Pulmonary embolus pearls in diagnosis:
We often use the Well's score for (PE and a separate for DVT), if the value is greater than 4 we consider v/q or CTPA. If less than 4 in the outpatient setting we consider D-Dimer which has GOOD negative predictive value (we can rule out PE).
When to consider someone's breathing is due to PE?
Clear chest x ray but low o2 saturation.
Risk factors for PE, specifically immobility, recent surgery within the past 3 weeks, active malignancy, history of PE.
The wells score also gives several points for no other cause best explains there shortness of breath.
V/Q scan is a great test and often undervalued amongst internal medicine residents, 2 features make it a poor test for our patient population occasionally
1. Abnormal cxr, patients with COPD often may have scarring evident on CXR, making it difficult to interpret the V/Q as there will be some V/Q mismatch.
2. Someone who is unable to inspire (as in someone with cognitive impairment).
** after a negative CXR, V/Q is the ideal test for pregnant patients.
ECG - most often sinus tachycardia, but we should always order it as a new RBBB, tall R wave in V1, the classic but rare S1/Q3/T3 and ST changes in anterior leads.
Blood gases for PE - may just show hypoxia, but in a patient with a COPD exacerbation whose PCO2 is 5 mmHg less than their baseline... consider PE.
Can you get pleural effusion? Yes! More often with chronic PE, but don't forget this on your differential of pleural effusion, it would usually be exudative.
CTPA - in some larger studies in patients with PE, about 20% of the time they were looking for PE, alternative diagnoses were made. Unfortunately, we now have an issue of picking up incidental subsegmental PE because CTPAs are too good for their own good!
There is debate how to treat these, often expert opinion is recommended, people generally treat patients with symptoms, or consider doing an US of the legs to see if a more impressive DVT is present when deciding to treat.
Finally, refer to the PERC score
http://www.mdcalc.com/perc-rule-for-pulmonary-embolism/
this is a scoring system that if negative, you may NOT even order a D-dimer, on room air, less than 50 years of age, no history of dvt (MEANS.... its probably not PE).
As I was not aware of the syncopal episode, I gave an approach to shortness of breath :)
Basically, heart, lungs, low hemoglobin and anxiety are the causes of shortness of breath.
Heart:
a. endocardium (valvular disease - aortic stenosis, aortic regurg, mitral stenosis, MR)
b. conduction system issues,
1. bradycardia - sick sinus, AV blocks,
2. Tachycardias - a-fib, aflutter, AVNRT, also VTs
b. myocardium
1. systolic failure (secondary to CAD, etoh, HTN, viral causes)
2. Diastolic failure (HTN, AS, HOCM).
c. CAD - shortness of breath can be an angina equivalent, mechanism is ischemia stiffens the myocardium, increasing pressures in the pulm circulation.
d. pericardium - tamponade, constrictive pericarditis
Lungs:
1. Alveol:
a: pulmonary edema (HF, ARDS)
b: pneumonia
2. Airways
a. Suprathoracic - laryngeal edema, or tumor (generally normal oxygenation, STRIDOR - generally inspiratory high pitched sound)
b. Intrathoracic - asthma, COPD
3. Blood vessels
a. Pulmonary embolus
b. primary pulmonary hypertension
4. Pleural
a. pneumothorax
b. pleural effusions (transudative/exudative)
5. Interstitium
a. edema
b. inflammatory
1. Organic exposure (hay, cotton)
2. Mineral exposures (asbestos, silicosis, coal)
3. Idiopathic disease (sarcoid, lupus, slceroderms)
Anemia
When any adult patient comes into the emergency room with shortness of breath we always start with vital signs, ABCs and make sure they are stable. History, physical exam and then are starting point would be CXR, ECG, and hemoglobin (this are simple tests that can dramatically change management).
We discussed some Pulmonary embolus pearls in diagnosis:
We often use the Well's score for (PE and a separate for DVT), if the value is greater than 4 we consider v/q or CTPA. If less than 4 in the outpatient setting we consider D-Dimer which has GOOD negative predictive value (we can rule out PE).
When to consider someone's breathing is due to PE?
Clear chest x ray but low o2 saturation.
Risk factors for PE, specifically immobility, recent surgery within the past 3 weeks, active malignancy, history of PE.
The wells score also gives several points for no other cause best explains there shortness of breath.
V/Q scan is a great test and often undervalued amongst internal medicine residents, 2 features make it a poor test for our patient population occasionally
1. Abnormal cxr, patients with COPD often may have scarring evident on CXR, making it difficult to interpret the V/Q as there will be some V/Q mismatch.
2. Someone who is unable to inspire (as in someone with cognitive impairment).
** after a negative CXR, V/Q is the ideal test for pregnant patients.
ECG - most often sinus tachycardia, but we should always order it as a new RBBB, tall R wave in V1, the classic but rare S1/Q3/T3 and ST changes in anterior leads.
Blood gases for PE - may just show hypoxia, but in a patient with a COPD exacerbation whose PCO2 is 5 mmHg less than their baseline... consider PE.
Can you get pleural effusion? Yes! More often with chronic PE, but don't forget this on your differential of pleural effusion, it would usually be exudative.
CTPA - in some larger studies in patients with PE, about 20% of the time they were looking for PE, alternative diagnoses were made. Unfortunately, we now have an issue of picking up incidental subsegmental PE because CTPAs are too good for their own good!
There is debate how to treat these, often expert opinion is recommended, people generally treat patients with symptoms, or consider doing an US of the legs to see if a more impressive DVT is present when deciding to treat.
Finally, refer to the PERC score
http://www.mdcalc.com/perc-rule-for-pulmonary-embolism/
this is a scoring system that if negative, you may NOT even order a D-dimer, on room air, less than 50 years of age, no history of dvt (MEANS.... its probably not PE).
Saturday, 14 March 2015
Thursday March 12th, GI bleed
We had a case of low hemoglobin in the setting of melena stools.
Some things to highlight.
We are becoming more excited about restricted transfusion, Villanueva and colleagues published a trial in the NEJM that assessed patients with acute GI bleeds and compared a restricted <70 to a liberal <90. Patients were excluded at the physician's discretion - thus VERY unstable patients who were exsanguinating were likely excluded.
They ended up with 444 patients in the restrictive strategy and 445 in the liberal strategy group
Interestingly, patients with cirrhosis were included
Some things to highlight.
We are becoming more excited about restricted transfusion, Villanueva and colleagues published a trial in the NEJM that assessed patients with acute GI bleeds and compared a restricted <70 to a liberal <90. Patients were excluded at the physician's discretion - thus VERY unstable patients who were exsanguinating were likely excluded.
They ended up with 444 patients in the restrictive strategy and 445 in the liberal strategy group
Interestingly, patients with cirrhosis were included
Mortality
Mortality at 45 days was significantly lower in the restrictive-strategy group than in the liberal-strategy group: 5% (23 patients) as compared with 9% (41 patients) (P=0.02)
We use different storing systems (The Rockhall had LHSC) to decide how soon someone should go for scope. Upper endoscopy is always easier to do then lower, and we also know that lower GI bleeds are more likley to stop bleeding on there own.
The basic management of ABCs, cardiac monitor, 2 large bore IVs, always applies!
Classic therapy of PPI 80 mg bolus then 8 mg/hr is standar of care until scope. The increased pH helps platelets clot. We have smaller trials looking at BID PPI therapy instead of an infusion but guidelines have not changed yet.
After the patient gets an upper endoscopy, we look to see for high risk features, referring to the forrest classification for the risk of rebleed, visible vessel, active bleeding, adherent clot are all features that are high risk. We would generally keep them on PPI and NPO for 48 hours in case they would need to be re-scoped.
Gastric ulcers need to be biopsied, duodenal ulcers - should check for H. Pylori but may not want to biopsy in the setting of fresh bleed, consider empiric therapy, vs follow up with ureas breath test.
Wednesday March 11th, elevated liver enyzmes
A classic internal medicine topic is elevated liver enzymes. Patients can have this picked up by the family doctor or can come in the hospital feeling unwell.
We discussed liver enyzmes vs liver function tests.
Liver function
INR - coagulation
Bilirubin - produce in the liver, stored in the gallbladder, helps emulsify fats for digestion, ultimately gives stool its brown colour
Albumin - helps with oncotic pressure, binds a variety of hormones
Breaks down toxins (thus potentially getting encephalopathic)
Gluconeogenesis - hypoglycemia common in fulminant hepatic failure
Enzymes
AST - also present in skeletal and cardiac muscle
ALT - more specific to the liver
Alk phos - cholestatic pattern, also comes from bones, osteoblastic activity, placenta
GGT - cholestatic but also increased with ETOH consumption,
LDH - present in all cells, but will be elevated in hepatocellular damage
Our generally approach is looking for a hepatocellular vs cholestatic patterns, the latter having more increased alk phos and bilirubin.
Ultrasound can show dilated ducts to suggest obstruction.
The Thousands club
The differential for elevated liver enzymes is impressive and with all cases you should probably pull up the list while you consider differentials in your patient.
Patients with liver enzymes in the thousands points us in a particular differential:
hepatic vein or portal vein thrombosis (budd chiari), viral hepatitis (hep A, B, EBV, CMV), drugs (tyelnol, isoniaizd, go over all new meds), ischemic (episodes of hypotension), autoimmune, wilsons disease (apparently).
Of note, alcohol alone will essentially NOT cause enzymes to be greater than 1000, so even if positive, look for other causes!
Of note, alcohol alone will essentially NOT cause enzymes to be greater than 1000, so even if positive, look for other causes!
Im sure there are case reports of things like hemochromatosis presenting the thousands, but your ferritin will be elevated with "inflammation" so thus a tsat of >55 could lead you in that direction.
The American Gastroenterology association is coming out with new guidelines in 2016, Canadian guidelines are really old, and AAALD don't have guidelines directly about elevated liver enzymes.
Here is a decent review published in 2011 on elevated liver enzymes
http://www.aafp.org/afp/2011/1101/p1003.html
The American Gastroenterology association is coming out with new guidelines in 2016, Canadian guidelines are really old, and AAALD don't have guidelines directly about elevated liver enzymes.
Here is a decent review published in 2011 on elevated liver enzymes
http://www.aafp.org/afp/2011/1101/p1003.html
DKA Tuesday March 10th
Tuesday we talked about diabetic ketoacidosis. Much more commonly in a type 1 diabetic and due to a lack of insulin. The body cannot turn off breakdown of fatty acids and excessive acetyl coa gets converted to ketones in the liver. The body also cannot take up glucose because insulin is needed for GLUT4 receptors (which are present on cardiac and skeletal muscle, as well as adipose cells).
Crucial points!
1. Look to the anion gap, a normal glucose, a normal pH does NOT rule out DKA. With increasing obesity, a 20 year old obese male could be mistaken for a type one. For every 10 of albumin that is below 40, add 3 to the anion gap.
i.e. If the AG is 12, but albumin is 30, the gap is really 15 (thus elevated!)
2. Patients are often volume deplete, so 2 large bore IVs and start fluids!
3. Do NOT start insulin until you have confirmed potassium level, start insulin and giving potassium when results are high normal (5.1). Withhold giving insulin if potassium is less than three.
4. Advising patients about sick takes: more frequent blood sugar checks, NEVER stop long acting insulin
Below is a link to guidelines from the Canadian Diabetes Association, they have detailed easy to read power points, a great resource!
http://guidelines.diabetes.ca/fullguidelines/Chapter15
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