A few more points on Community Acquired Pneumonia (CAP)...

Today we discussed our approach to CAP, however; I wanted to include a few more points that we didn’t have a chance to cover.

Always consider Complications of CAP:

·       Pulmonary: ARDS, parapneumonic effusion, lung abscess +/-cavity +/- necrotizing pneumonia, empyema, pleuritis, hemorrhage

·       Extra-Pulmonary/Systemic: hyponatremia, sepsis, purulent pericarditis

Always consider reasons why the CAP is not resolving:

·       Non-infectious: malignancy—bronchoalveolar carcinoma/lymphoma, COP, hemorrhage

·       Non-bacterial: viral, fungal

·       Immune-compromised host: atypical bugs not covered;

·       Wrong Antibiotic Coverage: Antibiotic resistance

·       Pneumonia complications (abscess, empyema, ARDS)

Non-Pharmacological Management

After discharge from hospital, be sure to consider the following for your patient:

1)    Follow-up CXR (PA and Lateral): used to assess for radiographic resolution of the CAP. Some authorities recommend a follow-up CXR, 6 weeks after treatment for patients >40 years who are smokers, to document radiographic resolution and exclude underlying sinister disease (i.e. malignancy). Note that the duration required before radiographic resolution varies based on the individual patient. In the young, otherwise healthy patient with normal cilia, expect radiographic resolution in 3-4 weeks. In older adults, particularly smokers or those with known ciliary dysfunction, radiographic resolution may take 6-8 weeks.

2)    Vaccination: recommend the annual influenza vaccine and the pneumococcal vaccine (if over the age of 65; or poor immune status, smoker, pre-existing lung disease). A booster is required for the pneumococcal vaccine q5 years.

3)    Optimize lung disease management: if the patient has Asthma or COPD, they should have regular follow-up in place, optimization of their medications, education surrounding exacerbations and Asthma Action Plans.

4)    Smoking Cessation: bring it up, assess their readiness and propose ways to cut down or quit!

Interesting Article- "Cardiovascular Events & Intensity of Treatment in Polycythemia Vera"

Hi everyone,

This article was recently presented by one of our PGY2s at Critical Appraisal. If you missed it, or if you're interested in Hematology, it's a great read!

Here is the link:

http://www.nejm.org/doi/full/10.1056/NEJMoa1208500

-Jade

Status Epilepticus- a recap of management!

Recap of the Management for Status Epilepticus (SE)...

First off, recall why Status is an Emergency: 

1) Risk of Systemic Complications: aspiration pneumonia, respiratory distress, hyperthermia, hyperkalemia, lactic acidosis, AKI, hypoxic brain injury, neurogenic pulmonary edema, etc 

2) Potential Neurological Sequelae: some studies in baboons who were intubated, paralyzed and in status epilepticus, demonstrated cerebral changes suggestive of ischemia in the grey matter. This may suggest that prolonged epileptic activity may cause neuronal injury independent of the systemic complications that arise...

(Journal Abstract: http://archneur.jamanetwork.com/article.aspx?articleid=572289)

3) Duration of Seizures: longer duration may result in more resistance with respect to treatment...

Some retrospective studies have demonstrated that patients that respond to first-line therapy often had a shorter total duration of seizure activity prior to successful treatment that those who did not respond to initial first-line measures. This may suggest that the longer the duration of SE, the more refractory a patient may become to treatment.

(Journal Abstract: http://www.neurology.org/content/43/3_Part_1/483.abstract)

Management: assess ABCs, IV access, monitored setting, neuroVS and regular VS; order stat blood work while managing (i.e. Stat Accucheck blood glucose, electrolytes, Ca, Mg, PO4, Albumin, AST, ALT, GGT, ALP, INR, Bilirubin, CK, TSH, toxicology screen, EtOH serum level, anti-epileptic drug level).

Other considerations (things to order once more stable): 12-lead ECG, troponin/Ck, CT head (*may consider MRI to better delineate soft tissue structures, depending on CT head results), EEG, +/- Lumbar Puncture (if consideration of CNS infection, such as meningitis)

ACUTE SEIZURE CONTROL: ABCs, IV access

1^st line- Benzodiazepine: lorazepam 1mg -2mg IV/SL PRN, up to total of 0.1 mg/kg. Can also be given IM; Diazepam 0.1-0.3 mg/kg IV. Diazepam can also be given rectally (10 mg PR x1, if no IV access)!!!

·       MOA: increase [Cl]- conductance in CNS GABA RC—decreasing neuronal excitability

2^nd line-Phenytoin (Dilantin) 15-20 mg/kg IV loading dose (maximum rate of 50 mg/minute for the infusion); maintainence 100 mg IV q8h

·       Benefit: efficacy in preventing recurrence of SE for extended period

·       NOTE: Modify infusion for hypotension, arrhythmia, pain/injury at infusion sites. The patient should be in a monitored setting and on a cardiac monitor!

·        DRAWBACK: must be dissolved in propylene glycol to remain soluble in IV form; Propylene glycol is the cause of most AV block and hypotension. It is also thought to cause “purple glove syndrome” resulting in pain, swelling and discoloration of the limb at the infusion site

·       MOA: stabilizes the neuronal membranes; decreases seizure activity by increasing efflux or decreasing influx of Na+ across the cell membrane in the motor cortex during generation of nerve impulses; shortens the action potential in the heart

Fosphenytoin= a pro-drug to phenytoin that is highly water soluble, thus, unlikely to precipitate during IV administration and reduced rate of local irritation

·       -Express dose in phenytoin sodium equivalents (PE)

o    i.e. 15-20 mg PE/kg at 100 mg PE/min

3rd line- Barbituates: similar to benzos, with a MOA of binding to GABA A RC, amplifying action of GABA by extending GABA-mediated Cl channel openingà increase Cl- outflow across membraneàneuronal hyperpolarization

Phenobarbital: administration is slow, causes prolonged sedation

·       Higher risk of hypoventilation and hypotension

·       Dose: 10- 20 mg/kg loading dose, infuse at 50 mg/min *(slower in elderly), may repeat dose at q20 minute intervals as needed (to maximum 30 mg/kg)

·       Monitor cardio-resp status! May need an ETT…

4th line- Propofol: a general anaesthetic 

·       Risk: Metabolic acidosis, renal failure, rhabdomyolysis, cardiac dysfunction

·       MOA: short acting, lipophilic IV GA, that causes global CNS depression through agonism of GABA A RC and perhaps reduced glutametergic activity via NMDA RC blockade

·       Dose: 1-2 mg/kg bolus IV, then 2-10 mg/kg/h

·       These patients typically have a definitive airway and are in the ICU!

Watch out for Lithium!

We recently had a case involving high serum lithium concentration. I wanted to recap some of the main points with respect to this...

Lithium Poisoning

Lithium- it is rapidly absorbed by the GI tract soon after oral administration with peak blood levels being reached in 1-2 hours after ingestion of immediate release (IR) products, and later (i.e. 4-6h) after sustained release products

·      It’s a small molecule with no protein or tissue binding and is therefore amendable to hemodialysis

·      It is excreted almost entirely by the kidneys! It is freely filtered but >60% is reabsorbed in the proximal tubules!

    What can increase Lithium absorption (i.e. increase serum level)?

·      Volume depletion, renal impairment/AKI

o   i.e. GI loss (gastroenteritis), diuretic use, AKI (i.e. NSAIDs, volume loss or other nephrotoxic drugs, ACEi/ARB)

o   Reduction in effective circulating volume (i.e. heart failure, ascites)

o   Elderly: lower GFR and reduced volume of distribution (have reduction in total body water and lean body mass)

Clinical Presentation:

·      Can be acute or chronic

Acutely, focus on the history if the patient is stable

·      PMHx, Meds, Dehydration/recent illness, type of lithium (IR, SR), infectious symptoms, co-ingestants, nephron-toxic meds

·      Symptoms: nausea, vomiting, diarrhea, palpitations, inquire about pre-syncope or syncope; neurological symptoms (develop late in acute poisoning as there is time for drug absorption into the CNS)—patients describe feeling agitated, confused, a bit sluggish; can also have tremor (coarse), fasciculations or myoclonic jerks, seizure, encephalopathy

Labs:

·      Obtain Serum Lithium concentration, CBC, Electrolytes, renal function (Cr and urea);

o   Lithium can elevate WBC count

o   Normal therapeutic lithium level is 0.8-1.2 mmol/L

o   Na: nephrogenic diabetes insipidus is a complication of chronic lithium use

·      Extended Lytes

o   Calcium abnormalities can occur

·      TSH: can have associated hypo- or hyperthyroidism

·      Check Serum Blood Glucose

·      Acid-base disorder: not typical; if present, consider co-ingestants

o   Toxicology screen (urine), salicyclate, acetaminophen level

·      12 lead ECG: can appreciate cardiac arrhythmia, hypotension, sinus node dysfunction, bradycardia, inverted T-waves (reversible!)

·      Beta-hcg if child-bearing age

Treatment: start with ABCs and ensure the patient is stable!

Specific treatment: IVF to maintain adequate renal function and replace losses if recent GI loses

·      Hydration: IVF (i.e. 0.9NS), watch the Na

·      GI Decontamination: oral activated charcoal does NOT prevent absorption of lithium (which is charged); thus, it has NO role in the management of an isolated lithium ingestion

·      Whole Bowel Irrigation with PEG may be effective in those with large acute ingestions (especially if it was a SR product)

·      Hemodialysis: Lithium can be dialyzed! Treatment of choice for severe toxicity

o   i.e. Lithium concentration >4 mmol/L

§  or >2.5 mmol/L with signs of significant toxicity (i.e. seizures, depressed mental status, cannot tolerate IV fluid hydration secondary to profound CHF, etc)

§  CALL NEPHRO IF IN DOUBT!