Sunday, 24 May 2015

Tuesday May 26th, approach to patient with chest pain, cavitary lesions

On Tuesday John gave me a fresh case that came in and we talked a bit about how to approach patients.

On internal medicine we see patients after they are referred. This is important because it helps us think about the two people we are working for. One is physician that consulted us - where we describe Reason for Referral (RFR for cool people). Next is the patient, who has a chief complaint, which may or may not be related to the reason for referral. Both of these issues should be addressed in our note.

Sometimes, we will not focus on a chief complaint if we feels its irrelevant, for example:
Chief complaint: "I ran out of animal crackers"

we probably don't need to pursue the details of this, but possibly pursue the route of psychosis.

John presented a male who had a history of chest pain: A discussion about the symptoms took place where we talked briefly about "must not miss diagnoses". So for example with chest pain
MI
Aortic dissection
Pneumothorax
PE
Esophageal rupture
Tamponade

Sucking chest wound is also life threatening

Although the above there own ways of presenting, have a low threshold for a CXR and ECG for all of the above when seeing patients in hospital as this will pick up the above the majority of the time (or at least make you suspicious of this).

In addition to thinking about life threatening causes/ "must not miss" diagnoses, it is also important to consider things that are not high yield, but we have cheap tests to pick them up, have good positive predictive value, and of course, change management.

For example, ordering an ecg in a patient with abdominal pain, although MI is low on the differential, it is possible, and if ECG were positive this would completely change our management of the patient.


Back to our patient, he came in with chest pain, some shortness of breath, fevers and chills, and was tachycardic when he presented. CTPA was initially ordered as chest x ray was quite unrevealing. Although the patient did not have a PE (and i think in this context this was a reasonable test to order), His Ct scan showed some peripheral cavitary lesions.

Approach to cavitating lesions is like most differentials

Infections: TB is the MUST NOT MISS (hence the patient was put on airborne precautions). Septic emboli from IE. Fungal infections.
Auto-immune: vasculitis, specifically Wegener’s
Malignancy: lung cancer or metastasis- usually metastasis is at the bases of the lungs as that’s where more blood flow is.
Congenital:

Mnemonic
·       C: cancer 
o   bronchogenic carcinoma: most frequently SCC
o   cavitatory pulmonary metastasis(es): again most frequently SCC
·       A: autoimmune; granulomas from 
o   rheumatoid arthritis (rheumatoid nodules) etc.
·       V: vascular (both bland and septic pulmonary embolus)
·       I: infection (bacterial/fungal)
·       T: trauma - pneumatocoeles
·       Y: youth
o   CPAM

Here is a decent article on approach to cavitating lesions, it's a bit too lengthy but more as a decent resource as they REALLY go into details of infectious causes
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2292573/

Wednesday May 27th Management of liver cirrhosis

On Wednesday, we talked about some management of ascities in the setting of cirrhosis.

Management of the underlying cause of cirrhosis (hepatitis hemochromatosis, etc), and approach to a patient with new onset ascites is a whole other topic on its own.

In general, all patients with new onset ascites should have a diagnostic paracentesis. When deciding on what to send this fluid for, consider the C’s as with taking fluid from anywhere else.

1.     CBC with diff (specically focussing on >500 WBC or 250 PMN for spontaneous bacterial peritonitis. A high amount of Red blood cells possibly suggestive of bleed/malignancy.
2.     Culture and gram stain: for SBP, E.coli, Kelbsiella, and Strep pneumo being the most common agents. If we see a polymicrobial culture one should consider secondary peritonitis (perforation in colon).
3.     Chemistry: Total protein and albumin, which is useful when we compare this to that in the serum. When commenting on a exudative fluid in ascetic fluid, it is actually more proper to refer to the SAAG, the serum ascities albumin gradient. A value >11 would imply a chronic process associated with increase portal pressures – a transudative process such as cirrhosis, heart failure, budd chiari, portal vein thrombosis. A SAAG < 11 would imply an acute inflammatory process and not typically associated with increased portal pressures: autoimmune disorders, nephrotic syndrome, TB, pancreatitis.
4.     Cytology: can be sent in new onset asicites especially when malignancy is being considered, yield is higher with sending three samples, however in a patient with chronic ascities due to liver disease, going in for a routine tap, this would be a waste of resources to send.
5.      
Of note choosing wisely Canada and American guidelines bring up that is not necessary to give FFP (for high INR) or platelets to these individuals as paracentesis carries a low risk of bleed and bleeding risk is more operator dependant rather than based on INR and platelets.
*note, this is different from high INR on warfarin

The pathophysiology of ascites is still somewhat controversial. Portal hypertension appears to be more a result of cirrhosis, and associated with ascities but actually not the cause. It is clear that there is splanchnic vasodilation, possible from an increase in nitric oxide in response to portal hypertension that may make liver capillaries more leaky. Also with lower splanchnic BP this likely causes kidnesy to reabsorb more sodium/water.

In morning report we talked about more chronic management of these patients as opposed to some of the acute complications (which I will briefly touch on at the end of this post).

1.     Screening for varices: It is recommended that patients with a new diagnosis of cirrhosis undergo EGD to screen for esophageal varices since these bleeds have a high mortality. With large varices, these can be banded to prevent future bleeds and a follow up EGD is usually done ~2 weeks after. Patients with low risk decompensated cirrhosis (liver function is ok, no ascities), might not need to be screened unless new symptoms/anemia develop. Beta blockers can be given for varices however some patients may not tolerate them as their baseline BP is low.

2.     Fluid balance: Lasix 40 spironolactone 100 is the classic ratio of diuretics, as that’s what’s been studied. Specifically the spironolactone can help with increasing potassium (which may be lowered by Lasix). Sodium of less than 2 grams of salt per day. Patients should get used to weighing themselves daily and be cognizant of increasing weight with abdo distension. Often patients should be educated how to increase their diuretics, to loose up to 1 kg/day if they have peripheral edema (500g without). Patients who are refractory to diuretics (after checking for adherence) may undergo large volume paracentesis ~2-4 weeks. Drains are not ideal as they can get infected. TIPS procedure done by interventional radiology is a way of bypassing the liver and may help refractory ascities, but can cause hepatic encephalopathy ~30%. Asking patients to stay on a restricted fluid diet is generally more realistic when they are hyponatremic from their liver disease  (sodium <130). This should be a conversation with the patient, if they can’t adhere to this, probably best to just increase their diuretics.

3.     Hepatic encephalopathy: There are different stages of this, coma being stage 4, that’s just no fun for anyone, patient’s that are confused can be checked for asterixis.. The mechanism behind this is also of debate, uptodate has like 6. Lactulose works, potentially by acidifying the intestines for ammonia to get turned into ammonium and can get excreted. So what do you do for these comatose patients? An NG tube can be put in, or a lactulose enema.  PEG can also be used as a relatively recent trial, the HELP trial http://archinte.jamanetwork.com/article.aspx?articleid=1907002
Showed that PEG actually helped resolved HE more quickly than lactulose. Patient’s who get HE without clear precipitants should be on this regularly, but choosing wisely guidelines in the states say this can be stopped if they were encephalopathy from a clear event. So… they may not have to be on this for life which is great for them because it tastes disgusting.

Other complications to pay attention to:
Patient with ascities that comes in with increased creatinine and sig. edema. DO NOT give them their diuretics, in the biggest concerns is hepatorenal syndrome, you need to check their urine (to make sure there is no ATN, GN,) and give them a fluid challenge! If there have tense ascities, may take off 4 liters, no more.

Patient with cirrhosis comes in with fever, abdo pain: rule out SBP! Will likely be on lifelone antibiotics after.

Patient with cirrhosis comes in with anemia, melena. Rule out upper GI bleed, triple therapy with octreotide (bolus 50 then 50 mcg/hr until scope) and PPI 80 mg bolus then 8 mg/hr until scope. And ceftriaxone 1 g daily to prevent SBP  - the only thing that has been shown to have mortality benefit in this situation.

Other pearl: It is generally recommended that you may remove 5 L via paracentsis without replacing albumin, after that we generally replace 6 g/kg of weight.  Our albumin comes in 100 mL 25% (25 g) bottles.


Baclofen can be used to reduce alcohol cravings in cirrhotics who continue to drink

Below is the choosing wisely recommendations from AASLD (American Association for the Study of LIver disease)


Below is updated 2012 recommendations form AASLD

http://aasld.org/practiceguidelines/Pages/guidelinelisting.aspx

Wednesday, 6 May 2015

April 29th COPD exacerbation, If you don't know, now you know

Our super star resident haifa talked about management of COPD exacerbation.

Please refer to previous article on approach to shortness of breath.

Firstly, on medicine you may have realized we don’t see many patients presenting with a new diagnosis of COPD. Often there is a previous diagnosis. It's crucial toconsider how that diagnosis was made.

Similarly when he hear “heart failure” we wonder about a recent echo, history of MI, leg edema, previous exacerbations, have they seen a cardiologist before, etc. So should the same be with COPD.
Also to consider ruling out other things that may change management such as… is this really asthma they’ve had a child or new adult onset asthma which may make us suspicious for vasculitis, bronchiectasis?

Diagnosis of COPD:
1.    symptoms compatible with it: SOB at rest, or exertion, cough +/- sputum, limitation of activity.
2.    Gold standard test to diagnose copd would be pulmonary function tests looking for an FEV1/FVC ratio <0.7 plus FEV1 <80% predicted with an incomplete response to short acting beta agonist (remember asthma involves >12% and 200mL improvement in FEV1 with bronchodilator)
3.    Absence of alternative explanation
A chest x ray is gernally part of standard of care

What about alpha one anti-trypsin?
- Consider in patients <45 years of age with COPD
- Predominance in the basilar areas of the lungs (as opposed to typical copd which is more in apices)
- minimal smoking history or no smoking history
- family history of early onset COPD or a family history of alpha one anti-trypsin deficiency.

To clarify, probably he most important thing we can do is counselling on smoking session (for asthma and copd). But in regards to pharmacologic treatment, considering an anticholinergic would be first line after ventolin for COPD, as oppose to inhaled steroids for asthma (this is commonly tested on exams).

So when someone with known COPD comes in with worsening shortness of breath, we consider this being an acute exacerbation. We’d expect worsening shortness of breath, wheeze, and productive cough. We would also want to know about infectious symptoms (fevers, chills, decrease po intake, N/V/D), medication adherence, lifestyle/environment (dust pollutants, cold air), CHF/pulm edema, ACS, pneumothorax, and post op related.
*note - ~25% of patients with COPD also have underlying CHF, have a low threshold for an echo when unable to explain decline in breathing.


Some physical exam findings we expect:

Early on: normal +/- prolonged expiration or wheezes on forced exhalation
With increased severity of obstruction: hyperinflation signs
·       Increased resonance on percussion (hyper-resonance): SN 32%, SP 94%, LR+ 4.8
·       Barrel Chest (increased AP diameter): SN 10%, SP 99%, LR+ 10
·       Decreased Cardiac Dullness on Percussion: SN 13%, SP 99%, LR+10
·       Match Test: requires patients to extinguish a lighted match held 10 cm from the open mouth. Failure to accomplish this is associated with a higher likelihood of airflow limitation. SN 61%, SP 91%, LR + 7.1
·       Sub-xiphoid cardiac impulse: SN 8%, SP 98%, LR+4.6
·       Pulsus Paradoxus (>15 mm Hg): SN 45%, SP 88%, LR+ 3.7
·       FEV1>9 seconds LR+ 4.8
·       Maximum laryngeal height <4cm; the distance measured between the top of the thyroid cartilage to the suprasternal notch at end of expiration: LR+ 2.8
End-Stage: may adopt positions to relieve dyspnea

o   Lean forward with arms outstretched and weight supported on palms or elbows
o   Accessory respiratory muscles (anterior scalene, SCM)
o   Expiration through pursed lips
o   Paradoxical retraction of lower interspaces during inspiration (Hoover’s sign)
o   Cyanosis;
o   Asterixis (4-6 beats/minute) due to hypercapnia
o   Cor pulmonale (elevated JVP, tender enlarged liver)—increased intra-thoracic pressure
o   Clubbing-NOT TYPICAL! (it is associated with ILD, Lung CA, bronchiectasis)

The Winnipeg criteria develop in the 80’s is used to decide if patient with COPD exacerbation are candidates for antibiotic therapy.
1.    increase sputum production
2.    increase purulence of sputum
3.    increase dyspnea

2 out of 3 makes the patient a candidate for antibiotic therapy in addition to steroids.


Acute Management:

Consider DDx: CHF, PE, Pneumoia, Aspiration, Metabolic, etc
Optimize lung function

1.OXYGEN & IV Access: supplemental O2 (target SpO2 88-92%); reduce pulm artery vasoconstriction, improve cardiac output
-Venture mask: preferred, to permit precise delivery of FiO2; can use nasal prong delivery for feeds
-Inability to correct hypoxemia with low dose FiO2: consider PE, CHF, ARDS, pulmonary edema, Acute Interstitial Pneumonia (AIP), severe CAP
-Re-assess frequently
2. GOALS of CARE: Discuss, as you may need NIPPV or Intubation/ICU management
3. MEDICAL MANAGEMENT:
o   INH SA BRONCHODILATORS (Beta-agonists & anti-cholinergics)
o   Ventolin: 2.5 mg NEB INH q1-4h PRN OR 4-8 puff by MDI with spacer q1-4h (while awake) prn
o   Atrovent: 500 mcg NEB q4h prn; 2 puff (18 mcg/puff MDI) with spacer q4h (while awake) prn
o   MDI vs NEB: during AECOPD, NEB may be easier to use
NOTE: in RCTs, NEBs are no more effective than MDI (when used properly!)
o   STEROIDS: decrease Length of Stay (0.5-2 days) & reduce treatment failure
o   Oral: rapid absorption, complete bioavailability, equally efficacious to IV
o   REDUCE TRIAL: compared 40 mg PO daily x 5 days vs 14 days—extending treatment duration did NOT reduce risk of recurrent exacerbation. We often give 50 mg daily as that’s how the pills come.
o   ANTIBIOTICS: indicated (i.e. Cefuroxime, Azithromycin, Levofloxaxin); some meta-analysis data suggest that Abx reduce treatment failure among inpatients, shorten LOS, and reduce mortality
o   MUCOACTIVE AGENTS: little evidence to support N-acetylcysteine
4. NON PHARMACOLOGICAL
o   Chest Physiotherapy: many techniques have NOT been shown to be beneficial…
5. MECHANICAL VENTILATION (NIPPV) - mortality benefit and decrease risk of intubation
-Trial may be needed in patients with AECOPD
-Indications: pH<7.3, RR>25, use of accessory muscles, hypoxemic *(must be alert, no facial trauma, no UBIG/Aspiration risk/copious secretions, HD instability, etc)
-R/A frequently and if no improvement in 30 min-1 h, move to intubation if goals of care allow
6. DVT Prophylaxis!
7. LT MANAGEMENT & FOLLOW UP
o   Education: Symptoms of AECOPD
o   Smoking cessation
o   Vaccinations: pneumovax, annual influenza vaccine
o   Exercise tolerance/rehabilitation
o   Review of puffer technique
o   Review of triggers
o   Treat other contributing illnesses or conditions (dysphagia, aspiration-SLP, GERD, etc)
o   Screen: Follow up with PFTs, 6 minute walk test, monitor BMI* (better outcome with less in patient admissions with overweight or normal weight)
o   LA agents: i.e. LA anti-cholinergic (Spiriva), LABA + ICS (Symbicort-budesonide & formoterol; 2 puff BID), SABA prn
o   Home O2 assessment with specific delivery of O2
·      PaO2< 55 mg Hg, or <60 mm Hg with cor pulmonale or Hct>56

People often quote a trial in 2006 in annals of internal medicine showing that 25% of unexplained COPD exacerbation, were screen to show pulmonary embolus. The three highest associations were history of DVT/PE, known malignancy, and a pCO2 5 mmHg below their baseline.  Thus if a patient is short of breath, wheezy, and is getting relief with ventolin, may hold of on that CTPA. D-dimer in this situation is tricky as it is generally designed for the outpatient setting and in the setting of inflammation (pneumonia) may be elevated.

Just as with cardiology, cardio rehab for patients post MI or severe CHF is ideal, so is the same with COPD with and is recommended with an FEV1 <50%, has not been shown to have mortality benefit but to improve quality of life. 

Please post questions or comments here to shake things up!