"Thrombocytopenia and an abnormal CXR"

In morning report we discussed the case of a young patient recently immigrated to Canada. As part of immigration they had routine bloodwork and a CXR done. The patient was called while at home with the results and advised to present to the nearest ER.

Referred to GIM for thrombocytopenia (platelet count of 26) and an abnormal CXR lesion NYD.

We discussed the DDx of low platelets, and those that would also tie in a potential abnormal CXR.


DDx of thrombocytopenia
1. Is it real? Look for clumping on blood film
2. Is it dilutional? (post massive transfusion/fluids)

3. Think: Decreased Production, Increased Destruction, Hypersplenism

Decreased Production

"Factory" problem
- congenital (TAR: thrombocytopenia with absent radii)
- bone marrow problem ie heme malignancies, solid tumours, fibrosis
- aplastic anemia
- MDS
- marrow suppression from sepsis
"Building block" problem
- nutrient deficiency (b12, folate)

Increased destruction

Microangiopathy
- TTP, HUS, DIC, HELLP, Malignant HTN, Scleroderma
Macroangiopathy
- valvular abnormality

Immune
Alloimmune
- PTP (posttransfusion purpura)
Autoimmune
- primary: ITP
- secondary: CTD (e.g. SLE), lymhoproliferative disoders, infections (eg HIV, EBV), drugs (e.g. sulfa, quinine)

Thrombocytopenia with an abnormal CXR? 
(before knowing what the CXR abnormality was)

Thoughts included SLE pericardial or pleural disease + thrombocytopenia.
Major thought was malignancy ie hematologic malignancy, with some sort of lymphoid mass (e.g mediastinal mass) + thrombocytopenia.
Infectious considerations included TB with abnormal CXR and marrow suppression from acute infection.

Coming back to the case, this patient had no significant PMH, was on no meds, OTC or prescribed, no illicit drug or alcohol use or smoking. No family history of signficant disease. Her history was signifcant for a 4 month history of easy bruising, skin changes, but significant bleeding issues. She had no symptoms of CTD, infection, no constitutional symptoms otherwise.

Her exam revealed an enlarged spleen as well as evidence of petechiae and ecchymosis on her extremities. She also had a ~1x1cm palpable, raised, blanchable lesion on her knee.

Lab investigations revealed
CBC: WBC of 16.9 ANC of 1.6, remainder counted as blasts. 
Blood film revealed myeloid blasts with evidence of Auer rods
CXR and subsequent CT revealed a spinal lesion first reported as possibly a neurogenic tumour  ....however in the context of the case, the thought was that this was a chloroma, or granulocytic sarcoma.

Her skin lesion on her knee might represent leukemic infiltration as well.

Unfortunately, as she recently came to Canada, she did not have coverage, but was initially managed in hospital and subsequently she returned back home to complete her investigation and management of her newly diagnosed AML.

A word or two on AML

Acute myeloid leukemia (AML) is characterized by an increase in the number of myeloid cells in the marrow with an arrest in their maturation, This often leads to hematopoietic insufficiency with subsequent decrease in other cell lines and the signs and symptoms they carry with it.

The clinical presentation of AML is diverse, but is attributed in large part to the signs and symptoms secondary to cytopenias (anemia symptoms, thromobocytopenia symptoms). 
It also presents with evidence of leukemic infiltration of tissues: ie liver, spleen, lymphadenopathy, and skin (leukemia cutis). It can also lead to a mass of immature cells termed granulocytic sarcoma, or chloroma.

Lastly, AML can present as an acute blast crisis with hyperleukocytosis. These patients require urgent management in an ICU setting, cytoreduction, fluids, as well as prevention/treatment of tumour lysis syndrome.

There are different subtypes of AML, most important to distinguish M3 or APL as the treatment is different.

Click here for a recent review article including treatment considerations for AML. 

Also see this NEJM review article, while from 1999, still nicely describes the clinical presentation.

"Never let the sun set on an empyema"

Today in morning report we discussed the case of a patient presenting with shortness of breath for one week.

PMH is significant for AL amyloidosis with renal involvement leading to a non-proliferative GN (aka nephrotic syndrome), as well as peripheral neuropathy.

Treatment includes a regimen of CyBor-D (Cyclophosphamide, Bortezomib, and Dexamethasone).

We touched on the topic of amyloidosis, understanding it is a disease of abnormal protein infiltration that can potentially affect any organ system and it can be either primary, or secondary (classically AL amyloid is seen with multiple myeloma, as well as chronic inflammatory disease). 

Thinking laterally, before any further information was given some thoughts were that this patient may have restrictive cardiomyopathy from his amyloid and now presenting in CHF. Another thought was this patient is prone to thromboembolic disease given his nephrotic syndrome and may be presenting with a PE. Lastly given his immunosuppresive therapy, this may be an infectious etiology. Specific thought was given to thinking of PCP if he had been on longer term steroids. If the presentation was more chronic with associated constitutional symptoms, one would also put TB on the DDx.

Further history revealed no other localizing signs of infection save for a non-productive cough, no cardiac or CHF history, no risk factors for thromboembolic disease and no constitutional symptoms. ROS was significant only for some mild dysphagia on occasion. 

On exam he was afebrile, normal blood pressure, mildly tachycardic with a HR of 100. RR was 22 and he was saturating 95% on room air.
On respiratory examination he was in no distress, with dullness to percussion on the right, as well as decreased breath sounds on the right side.

Imaging showed a a large, almost complete white out of the right hemithorax. 
There was tracheal deviation away from the white out consistent with fluid as opposed to complete collapse.

CT chest showed a large pleural effusion with bubbles that raised concern for an empyema

Diagnosis:
Presumed oral aspiration (remember his history of dysphagia), possibly due to amyloid involvment, leading to empyema.

Ultimately the patient had drainage of frank pus, and the microbiology grew Streptococcus anginosus and Haemophilus parainfluenzae

Remember

Uncomplicated parapneumonic effusion: 

• slightly turbid 
• pH > 7.3 
• glucose > or equal to 3.4 
• ratio of pleural fluid to serum glucose > 0.5
• LDH < 700
• Negative micro

Complicated parapneumonic effusion: 

• cloudy
• pH < 7.2 
• glucose < 2.2 (some quote < 3.4)
• ratio of pleural fluid to serum glucose < 0.5 
• LDH > 1000 
• Micro may be positive

Empyema

• pus
• positive micro

A word on Streptococcus anginosus aka Strep milleri

- Very "abscess-ogneic" (other bacteria that are abscess-avid....hypermucoviscous klebsiella, anaerobic bacteria such as bacteroides fragilis)

- Has a caramel smell in the micro lab

Treatment in this case, if it was truly only S.anginosus could be high dose penicillin. However, given the additional micro findings as well as possibility of polymicrobial infection with oral anaerobes, it was determined that covering for anaerobes as well is reasonable. 

Check out this clinical practice article on the diagnosis and management of parapneumonic effusions and empyema.

Click here for a CMAJ article on parapneumonic effusions.

Managing Meningitis 

This topic was discussed in noon rounds today as part of our emergency lecture series. 

Bacterial meningitis is a medical emergency - data from a retrospective study in 2008 from the Journal of Infection showed that unfavourable outcomes increase by 30% for every one hour delay in treatment. From med school and residency, we know that it requires antibiotics (and maybe steroids) targeted at the appropriate organisms, we know that some people may need a CT scan, and we know that it is diagnosed with an LP. The order in which we do all of this, or if we need to do them all is sometimes unclear.

Firstly, is there physical exam findings that can help rule in our out? From the 1990 JAMA RCE article "Does this adult patient have acute meningitis?" we know that the absence of all 3 of fever, mental status changes, AND neck stiffness is quite sensitive in ruling out meningitis. Also a negative jolt accentuation has good sensitivity as well. There is no physical finding that is diagnostic and definitive diagnosis requires further testing.

Secondly, what about a CT head before an LP? Practice guidelines, including those from the IDSA, would suggest that select few patients can safely undergo LP without prior CT. Essentially these are people who lack any features including age > 60, immunocompromise, prior history of CNS infection, recent seizure, objective focal neurologic findings.

If you do send someone for a CT scan, they should be started on therapy as time will add up as you await transport, the scan, and the interpretation. This invariably leads to concern that we will 'sterilize' the CSF and lose the ability to make a definitive diagnosis.

We now know that the biochemical and hematologic abnormalities persist despite antibiotic therapy, at least within the first 24 hours, and possibly longer. This was first answered in 1990 when a noninferiority study comparing "the new" Ceftriaxone to Cefuroxime for the treatment of bacterial meningitis in pedatric patients. They performed LP's on presentation and 24 hours post antibiotics. While the rate of positive gram stains predictably went down, the other parameters such as WBC, protein, glucose, remained unchanged, and so could aid in diagnosis. 

The landmark NEJM study by deGans et. al in 2002 showed that dexamethasone improved outcomes and mortality for S.pneumo meninigitis, but given the low numbers, the same could not definitively be said for other pathogens.

Bottom line, as per guidelines, 

If bacterial meningitis is suspected and the patient does not have indications for a CT, 

then the order should be blood cultures, LP, empiric therapy.

If a CT is indicated, 

then the order should be blood cultures, empiric therapy before sending to CT, if CT negative, then LP.

Click here for the IDSA guidelines for bacterial meningitis

And here for a great summary on key points of bacterial meninigitis from the CMAJ.

Acute Kidney Injury

Today in subspecialty morning report (nephrology) we discussed an elderly patient who presented to the emergency department with a history of agitation, vomiting and a recent episode of dysuria treated with two courses of antibiotics. Referred for AKI and hyperkalemia.

Past history included alcohol use, depression, possible COPD, and spinal stenosis.

Medications included citalopram, quetiapine, and bisoprolol, as well as recent courses of TMP/SMX and Levofloxacin.

Aside:
Automatically think of TMP/SMX when hyperkalemia is brought up. The TMP component blocks ENaC and so acts like a K sparing diuretic and can cause hyperkalemia. Beta-blockers as well can theoretically worsen hyperkalemia (by inhibiting shift of K into cells)

Given his history of a recent urinary symptoms and now clinical deterioration, there was discussion whether this person could be presenting with persistent infection.

If he truly had a urinary infection recently, then it would be important to not only treat, but investigate the reason why this 91 year old male now has a urinary infection.

Given his history of spinal stenosis, the possibility of bladder dysfunction was raised as well.

Clinically he was afebrile and hemodynamically stable, although elderly patients can present atypically, and he is on a betablocker that may mask tachycardia. His exam was significant only for abdominal tenderness. He had no asterixis.

Aside:
Asterixis, a form of negative myolconus, and inbability to maintain sustained contraction, DDx:
- Hepatic encephalopathy 
- Uremic encephalopathy
- Hypercarbic encephalopathy

Labs were significant for a potassium of 7.1 and a creatinine of 1750 (baseline of 50). 

Remember that creatinine comes from muscle and so 'normal' depends on the person. Actively rising creatinine will overestimate GFR, and actively dropping creatinine will underestimate GFR.

Aside:
The question was raised as to whether he has underlying CKD.
One way to determine would be to U/S looking for small kidneys.
Although, there are causes of CKD with large kidneys
- DM
- PCKD
- Amyloid
- HIV nephropathy

He also had a mild Anion gap metabolic acidosis.

Aside:
AG = Na - (Cl + HCO3)
Normal depends on Albumin.
An albumin of 40, gives a normal AG of 12
The lower the albumin, the lower the normal AG (for every 10 decrease in albumin, ~ 2 lower AG)
Causes of AGMA (anion gap metabolic acidosis)
- Lactic Acidosis
- Ketoacidosis (diabetic, alcohol, starvation)
- Renal failure
- Toxins (methanol, ethylene glycol, ASA)

This is a classic example of the tried and true internal medicine approach to acute renal failure. Won't be discussed in detail here, but click here for a good CPC NEJM case that reviews the approach.

A bladder scan that revealed 1.5L of retained urine.

Treated for acute urinary obstruction and hyperkalemia

1. Hyperkalemia
- Calcium gluconate
- Shift with insulin and D50W (insulin to shift K into cells, D50W to avoid hypoglycemia)
- Facilitate excretion - treated his acute urinary obstruction

2. Obstruction
- With a foley inserted he diuresed and his creatinine fell 500 points within hours and ultimately improved to his baseline of 50. Gratifying case and he did not need dialysis.
- He is being investigated as to the cause of his obstruction.

"The only real difference between medicine and poison is the dose...and intent"

- O. Hernandez MD

Today in morning report we discussed a case of a patient referred after having a fall, and being unable to ambulate. 

We discussed our own personal assumptions that arise when given consults and that we should always stay open minded and be sure not to be biased when seeing patients. Especially in this case where one might have assumed a non-urgent case that suddenly became very urgent.

Upon assessment, this patient was noticeably drowsy, lethargic, slow to answer, and according to her RN in ER, this was a change from initial presentation. 

PMH revealed bipolar affective disorder, congenital bllindness, overactive bladder and restless legs syndrome.

Meds included risperidone, quetiapine, amitriptyline, tolteradine, bupropion, clonazepam.

On exam afebrile, BP 140/70, HR 88, RR 22 but would jump up to >50. Patient was diaphoretic
Neurologic exam revealed a depressed mental status, increased tone on exam with cogwheel rigidity in the upper extremities and lower extremity rigidity. Question of tremors on exam or clonus, it was unclear. No inducible clonus, Reflexes were difficult to illicit because of the rigidity.

Labs revealed an elevated CK at 43000 and elevated liver enzymes. Imaging, ECG were all normal. 

Given this history and presentation and especially her meds, we generated a list that included:

1. NMS (Neuroleptic malignant syndrome)
2. Serotonin Syndrome
3. Anticholinergic toxicity
4. Combination

NMS is a result of dopamine blockade and is usually with typical antipsychotics, but can be with atypicals. It is an idiosyncratic reaction and can occur even with prolonged exposure. Risk factors include a change, or an increase in dose, high doses. Patients with PD and a sudden withdrawal of their meds can also get NMS. NMS is associated with fever, autonomic instability, rigidity, mental status change. Often is bradyreflexic and is usually not as acute as serotonin syndrome.

Treatment is supportive including active coolling, d/c'ing offending meds, and can consider dantrolene.

Serotonin syndrome is the result of a combination of increased release, inhibition of reuptake and/or inhibition of breakdown. We discussed MAOI's and how other medications can have MAOI effects e.g. Linezolid. Defining features include similar presentation as NMS, but often more acute, and with hyperreflexia and clonus. 

Treatment is supprotive, d/c'ing offending meds. Antidotes aim at blocking 5HT2 receptors i.e. cyproheptadine. Atypical antipsychotics also have 5HT2 blockade particularly olanzapine

Anticholinergic toxicity presents with fever, elevated BP (usually not that high), dilated pupils, confusion, and they are dry!!
We touched briefly on TCA overdoses, but mainly to state to monitor QRS, give bicarb if needed and to be careful in managing arrythmias and seizures with medications that further block Na channels. Also to avoid physostigimine in TCA overdoses because of risk of fatal bradyarrythmias. Clearly, a topic for another day.

Given her medications and presentation it was felt that this was either NMS or Serotonin Syndrome. 

Her med list favoured NMS over Serotonin syndrome as the only serotinergic medication she was on was bupropion which has small effects. Additionally she was also on quetiapine which might have given some 5HT2 blockade.

She was admitted on tele, ICU followed, psychiatry was involved and we discussed getting poison control/toxicologist in this case. 

Her course is that she is improving, starting to be more alert and admitted to taking an excess amount of pills, though this issue is currently being investigated.

Check out this review article on serotonin syndrome from the NEJM

Approach to the patient with cancer

Today we had an oncology morning report case.

We discussed a middle aged female with known metastatic cervical cancer to bone and pelvic lymph nodes, who presented to the ER generally unwell.

What is your approach to this patient? 
Oncology, especially advanced cancers, can often be intimidating and we often feel overwhelmed in managing these cases. In general, think easy, don't think hard....

The general approach is not too different than what we are normally used to, when thinking about these patients, go through the following:

1. Is this cancer related or cancer unrelated?

Then, if cancer related:

1. What is the complication? Is it reversible?

To generate this differential, think of "DIMS-H"

• D rugs: chemo vs non-chemo (ie steroids, opioids)
• I nfection: febrile neutropenia OR think of an infection secondary to some blockage ie biliary tract, urinary etc.
• M etabolic: Hyponatremia, renal failure, hypoglycemia, hypercalcemia, liver dysfunction
• S tructural: CNS mets, spinal cord compression, mass obstructing a lumen: PE, airway, GI (GOO, SBO), infiltration of organs (liver), fluid xs (CHF, pericardium, ascites)
• H eme: DIC, cyptopenias

2. What is the context? Curable or non-curable cancer? Goals of care?

Difficult discussions, but necessary.

Back to the case, this patient was unwell, no localizing symptoms or signs. She was no longer receiving chemotherapy. Her medications were Hydromorphone via CADD pump and Methadone. 

Aside: Methadone use in this context is for neuropathic pain relief. Gives insight that likely this patient has required a lot of analgesia and is likely being followed either by a palliative care physician or pain specialist. 

On exam she was mildly hypovolemic on exam. Labs showed a calcium of 3.3 with an albumin of 36. 

Aside: Quick calcium correction: for every decrease in albumin of 10 from normal (which is 40), increase the calcium by 0.2. 
e.g. if Albumin 40, then no correction. if albumin 30 and measured calcium is 2.0, then albumin is 10 below normal, therefore add 0.2 to calcium, which would give a corrected calcium of 2.2

We then discussed hypercalcemia of malignancy

Causes:

-          Primary hyperpara vs non-primary hyperpara

-          Primary hyperpara actually more common in patients with cancer so remember to check.

-          Non-hyperpara causes are malignancy associated, meds (HCTZ, Li), Granulomatous disorders

-          Think of malignancy type

-          Bony mets and local osteoclastic activity most common

-          Lymphoma often 1,25 Vit-D mediated

-          Solid tumours ie breast, squamous cell can be PTHrP mediated

-          Rarely is ectopic PTH from tumours a cause

Mechanisms:

1. Increased osteoclastic activity (local osteoclastic activity, PTH, PTHrP, ectopic PTH)
2. Increased renal Ca absorption (PTH, PTHrP, ectopic PTH)
3. Increased gut absorption (1,25 VitD, possibly PTH)

 -          (Some discuss role of RANKL activation ie in multiple myeloma)

Calcium and volume status

-          Cacliuresis leads to volume depletion

-          Hypercalcemia acts at Loop of henle, inhibiting sodium (and calcium) reabsorption leading to volume depletion. Acts like Lasix.

General rules

-          < 3 mild

-          3-3.5 moderate

-          > 3.5 severe

-          Primary hyperpara in isolation is usually mild

Hx:

-          “Bones, stones, abdominal groans, psychiatric overtones”

-          Volume status

-          Calcium and Vitamin D intake

O/E:

-          Really is primarily volume status

Labs:

-          Correction for albumin (10:2)

-          Check PTH

-          Renal

Treatment:

-          Stop offending meds

-          Stop xs PO intake of calcium, vitamin d

-          Fluids fluids fluids

-          Bisphosphonate (2001 J Clin Oncol showed Zoledronate superior in terms of faster onset, longer duration than Pamidronate….But Zoledronate more expensive, not clear how clinically significant these results were). There is concern if severe renal failure, but this is often with multpile doses, no recommendations to reduce the dose or slow infusion. Bottom line for the most part is give the bisphosphonate.

-          Calcitonin can be considered, but is short acting, can get tachiphylaxis

-          Lasix not routinely recommended given overall volume depletion. If overloaded then can give

-          Dialysis as last resort

-          Phosphate often low as well. Carefully replace, IV discouraged unless absolutely needed as can bind calcium and precipitate hypocalcemia

-          Novel ideas are use of RANKL inhibitors, PTHrP antibodies

-          Steroids have a role in 1,25 Vit D mediated disease.

Click here for the NEJM paper on hypercalcemia in malignancy

Infective Endocarditis

Morning report today was about a patient presenting with a 2 month history of fevers, sweats, and a recent stroke. 

Otherwise healthy and we discussed a differential that could tie everything together - this included:

- Infective endocarditis
- "non-infective" endocarditis such as Libman-sacks endocarditis seen with SLE
- Malignancy leading to a hypercoaguable state, as well as other myeloproliferative disorders
- Vasculitis 

Story revealed that due to fevers, the patient had received multiple courses of antibiotics with transient defervescence, but the fever would return soon after stopping antibiotics. Additionally, a TTE done during his initial presentation was normal. 

When the patient presented to the team's attention, was noted to have a systolic ejection murmur raditating to the axilla, still febrile and ultimately the diagnosis was felt to be concerning enough for infective endocarditis that another TTE was ordered. This time demonstrating a mitral valve vegetation. (Had this been non-diagnostic, then a TEE would have been pursued).

Making a diagnosis: Duke's criteria

Major Criteria:

1. Positive blood cultures for endocarditis

• typical microorganisms
• persistent bacteremia
• single positive culture for Coxiella burnetti (Q fever)

2. Evidence of endocardial involvement

• Echo evidence
• NEW regurgitant murmur

Minor Criteria:


1. Fever 
2. Predisposing cardiac lesion or IVDU
3. Vascular phenomena: arterial emboli, septic emboli, mycotic aneurysms, ICH, conjunctival hemorrhages, Janeway Lesions
4. Immunologic phenomena: GN, Osler's nodes (painful...think "Ooooowwsler's nodes"), Roth spots, positive RF
5. Positive blood cultures but not typical bacteria

Principles of management of IE

- Culture culture culture
- Unless evidence of sepsis, septic emboli, florid CHF, there is often not an immediate urgency to give antibiotics and you should always be sure that all microbiologic investigations are done before starting antibiotics.
- Most "culture-negative" organism can now be grown pretty well in our labs
- Prior antibiotic exposure is the biggest reason for culture negative IE
- Empiric antibiotics depends on native vs prosthetic valve and should target known organisms for IE

Indications for CV Surgery (in general, case-by-case)

- Heart Failure
- Uncontrolled Infection
- Prevention of emboli


Click here for a review of infective endocarditis from the NEJM 2013.
See the Supplementary appendix for suggestions of empiric therapy.

Transaminitis: a classic AM report

Morning report today was a case of a patient presenting with fever, abdominal pain, and a transaminitis over 1000.

We reviewed the case presentation focusing questions and looking for physical signs that center around our differential diagnosis.

DDx of liver disease in general

1. Drugs/Toxins
- Consider both prescribed and non-prescribed
- Acetaminophen being a classic example, as well as EtOH
2. Infection
- Viral hepatitis especially Hep A. B, C can be acute, but often more chronic picture. D is associated with B. E has high mortality in pregnancy. HIV, CMV, EBV, (VZV) all other viral causes.
- Bacterial infection more often associated with abscess, but less so with acute hepatitis in and of itself.
- Parasitic infections, an example is "Katayama fever", which is acute schistosomiasis
3. Vascular: 
- including ischemia (shock liver), cardiac cirrhosis (don't forget! look at JVP, ?TR)
- thrombosis either hepatic vein (Budd-Chiari) or portal vein
4. Metabolic: 
- Wilson's disease: think of in younger patients, with concomitant hemolysis, neuro-psychiatric symptoms 
- Hemochromatosis: think of if DM, heart disease, joint disease
5. Autoimmune
- "True" AIH, especially in patient with other autoimmune conditions
- PBC (females, 40s), PSC (hx of IBD)
6. Structural 
- Stones, CBD stone in particular
7. Malignancy
- Not often causing hepatitis
- Discussed rare cases of lymphomas causing hepatitis.

DDx of transaminitis > 1000
1. Ischemia
2. Infection 
3. Toxin
4. Stone
5. AIH

Ultimately this case focused on the DDx, the investigations were ordered for the above, all was ruled out, and given this patient's history of choledocolithiasis it was felt by our hepatology service to be in keeping with a passed stone. 

Incidentally the patient grew E.Coli bacteria in their blood and was treated in with beta-lactam antibiotics, and subsequently developed a mild cholestatic pattern of elevation. This has been well described with beta-lactams. The patient recovered during her hospital stay and was discharged home.

Check out this CMAJ review article  on elevated liver enzymes.

Bilateral leg edema

In morning report today we discussed a case of a  patient presenting with progressive bilateral leg edema.

Just based on this complaint alone we found that a differential was generated with cardiac, renal, hepatic, structural, and medication causes being cited first. 

As with any case, we will move from type A and type B reasoning to come to a conclusion. Analytical reasoning and pattern recognition will interplay in our minds as we work through a case.

This patient had signs and symptoms that were ultimately consistent with right sided heart failure in the absence of evidence of left sided disease.

Isolated right heart failure often raises the question of whether the person has pulmonary hypertension.

We went through clues for this on physical and investigations.

Physical exam findings of pulmonary hypertension include:

On inspection: an elevated JVP

On palpation of the precordium: Palpable P2, RV heave, thrill of TR

On auscultation of the precordium: Loud P2, widely split S2, TR murmur, right sided S3,4

ECG findings of pulmonary hypertension include

RBBB

P pulmonale

RVH

RAD

Additionally, one of his findings on exam was a pulsus paradoxus.

Remember that a pulsus paradoxus is the change in systolic pressure with respiration.

As we inspire, we increase right sided filling, and ventricular interdependence can lead to a shift from right to left and in pathologic situations, can lead to a decrease in left sided filling, and subsequently a decrease in CO. This explains why with inspiration, the Korotkoff sound disappears as there is no flow through the systemic circulation.

Remember there is a DDx to pulsus paradoxus including...

1. Pericardial disease

2. Cardiomyopathy

3. Severe RHF

4. Obstructive lung disease

In this person, we discussed ventricular interdependence and how increased filling pressures can lead to a right to left shift, and thus decrease CO.

This person did NOT have tamponade, and so gentle diuresis was carried out with improvement in his renal blood flow and decrease in his symptoms.

Important to note that in this case diuresis was appropriate, but in true tamponade, diuresis will decrease intraventricular pressures that are normally overcoming pericardial pressures and this can lead to hemodynamic collapse.

Toxidromes

Morning report on Wednesday July 10 was a case of toxic ingestion.

In the approach to toxidromes, there are some guiding principles.

1.) Is this an emergency?
2.) What did they take (think of co-ingestions), how did they take it, when did they take it
3.) Treatment consists in general of: Antidote if avaialble, decrease absorption, increase elimination, treat complications.

History is often difficult in these cases as the patient may be alone, and may have an altered mental status. Collateral, family, friends is key.

The physical exam is so important and often you will see tables breaking down toxidromes and the patterns on physical.

Key parameters are:
Mental status
Temperature
BP
HR
RR
Pupils
axilla

Major toxidromes are sympathomimetic, anticholinergic, cholingergic, opioid, and what I think of as others including serotonin syndrome, NMS.

Some (usually) defining features:

Anticholinergic: DRY as a chip!

Cholinergic: opposite, everything is leaking

Opioid: pinpoint pupils

Serotonin syndrome: hyperreflexia, clonus. Often is a faster onset than NMS.

This was a young female who had ingested 45 tablets of "222" which consists of codeine, caffeine, and ASA.

This case brought up the concern of both the codeine and the ASA.

She had no evidence of opioid overdose. As a side note, codeine as we know is metabolized by CYP2D6 to morphine. ~5-7% of Caucasians are deficient in CYP2D6, ~1% Asians. Some populations over express CYP2D6 and may run into problems of toxicity, or may require smaller doses. 

ASA toxicity can be difficult to manage as there is no specific antidote. Treatment principles include:

1. Monitoring of levels to ensure decreasing. Beware that ongoing absorption may occur.

2. Acid-base and electrolytes

Classically salicylate toxicity causes an anion gap metabolic acidosis and a respiratory alkalosis. 

Remember that HS ↔ H+  + S-  It is the neutral HS that can enter the CSF and tissues.

Thus treatment aims at alkanilizing the urine to keep in the anion form and prevent entry into tissue.

These patients can become neuroglycopenic so pay close attention to glucose.

3. GI decontamination

If appropriate and no contraindications activated charcoal or even whole bowel irrigation can be considered. Particularly in early cases.

4. Airway

Remember that the respiratory alkalosis is also helping maintaining alkalemia. Intubating a patient may worsen toxicity if hyperventilation is not maintained as the pH may drop and further push towards the neutral HS that can enter tissues. This is tricky as these patients may very well require intubation especially as their mental status deteriorates. Monitor the pH, minute ventilation, and pCO2

5. Enhancing elimination

As mention urine alkalnilization is part of this.

Dialysis ultimately is an effective means to eliminate.

This information and further detail can be found using the link below to the ACMT recently published recommended treatment guidelines/considerations for Salicylate Toxicity.

Also, always remember to call poison control, they can help tremendously!

http://www.acmt.net/_Library/Position_Drafts/Management_Priorities_in_Salicylate_Toxicity_APPROVED_03_13_13.pdf