AM Report 11/17/16: Empyema

Remember Light’s Criteria is SENSITIVE for picking up EXUDATES but mis-classifies ~25% transudative effusions as exudative!
-You only need to have ONE of Light’s criteria to call it an Exudate!

lights-criteria

TRANSUDATE
Remember the top 3 but there is an extensive list…

CHF (most common)
-Hepatic hydro-thorax from cirrhosis
-Nephrotic syndrome

EXUDATE 
Remember the top 3 but also has an extensive list…

-Malignancy
-Pneumonia
-Tb

What percentage of patients with bacterial PNA get an associated effusion?
>40 % and up to 60 % with pneumococcal PNA, and can be either uncomplicated, complicated, or empyema


Uncomplicated parapneumonic effusion

-Resolves with antibiotic treatment of PNA
-On CXR, must be free-flowing and <10 mm
-Very low risk, does not need drainage 

Complicated parapneumonic effusion

-Small/Mod  in size, >10 mm but <1/2 hemithorax
-Negative gram stain/culture, pH>7.20
-May need drainage based on clinical status

Complicated parapneumonic effusion (second type)

-Large >1/2 hemithorax, LOCULATED, thickened parietal pleura (high risk if thickened parietal pleura, suspect Empyema) 
-Positive culture or gram stain OR
-pH<7.20
-MUST drain effusion, moderate risk

EMPYEMA!

-defined as PURULENT appearance of pleural fluid OR
pH <7.20 (don’t forget to order pH and keep it on ice!)
-If ether of these exist, MUST drain effusion, highest risk, usually with tube thoracostomy (chest tube)

Treatment

-Empiric therapy should cover Gram + (eg: Staph, Strep), and Anaerobes (eg: Fusobacterium, Bacteriodes)
-Empyema is treated with 4-6 weeks of antibiotic treatment

empyema

AM Report 11/15/16: Hypocalcemia

Etiologies of a PROLONGED Qtc (not an exhaustive list) 
Remember that many LOW electrolytes can lead to prolonged Qtc increasing risk of arrhythmias (usually Torsades)

Drugs  (large category, includes anti-psychotics, anti-arrhythmics,TCA, anti-histamines)
-HYPOkalemia
-HYPOmagnesemia
-HYPOcalcemia
-HYPOthermia
-Congenital (eg: long QT syndrome)

What can cause HYPOcalcemia?

-HYPOparathyroidism (PTH controls calcium and phosphorus homeostasis)
-HYPOproteinemia (Pearl: always check albumin with calcium unless you are checking ionized calcium!~0.8 increase in calcium for every 1.0 decrease in albumin from 4.0)
Renal disease (remember that the kidney makes activated Vit D with 1 alpha hydroxylase and Vit D absorbs calcium from the gut)
-Vit D deficiency (cannot absorb calcium)
-Hyperphosphatemia (binds calcium and lowers serum levels, is the etiology of hypocalcemia in Rhabdo and TLS)
-Acute Pancreatitis
-Chelation (eg: after being given Citrate/EDTA/Foscarnet)
-Hypomagnesemia (Mg needed for PTH activity)
-Hungry bone syndrome (seen after parathyroid surgery for elevated PTH where bones start sequestering the calcium levels in the serum)

Clinical manifestations of HYPOcalcemia

Remember CATS mnemonic!

hypocalcemia-signs-and-symptoms-nursing-acronyms

NEUROMUSCULAR IRRITABILITY 

-Parethesias
-Tetany
-Trousseau’s sign-carpopedal spasm seen when inflating BP in upper arm above systolic pressure (highly sensitive and specific!)
-Chvostek’s sign- facial twitching in response to tapping over facial nerve (absent in one third of patients with hypocalcemia, and seen in 10 % of patients with normal calcium levels!)-Bronchospasm/Laryngospasm

CARDIAC

-Prolonged Qtc, Arrhythymia
-Hypotension, HF

NEUROLOGIC

-Seizures
-Extra pyramidal symptoms (eg: Parkinsonism)
-Irritability, depression, personality changes

PRIMARY vs. SECONDARY vs. TERTIARY HPT 

Where does the problem start? 

Primary– Elevated PTH is the problem leading to high Ca, low Phos
Secondary-LOW calcium is the problem leading to elevated PTH
Tertiary-PTH is again the problem but it is functioning autonomously due to uncontrolled secondary PTH or post-renal transplant so calcium is elevated but phosphorus still elevated due to renal failure.

pth-table

AM Report 11/16/16: RLQ Pain

NuvaRing:

  • Combined (progestin/estrogen) hormonal contraceptive vaginal ring
  • Works by preventing ovulation and inhibition of sperm penetration (via cervical mucosal changes)
  • Used for a 3 week period followed by a “break week;” reported 91% effective with typical use

Appendicitis:

Epidemiology: Most common indication for emergent abdominal surgery in childhood (<14 years old); Males > Females.

Pathophysiology: Non-specific obstruction of the appendiceal lumen (fecal material, undigested food, enlarged lymphoid follicle, etc.)

Clinical Manifestations: Anorexia, periumbilical pain (early) → migration to RLQ (often within 24 hours), vomiting (after onset of pain), fever (24-48 hours after symptoms)

Diagnosis: Clinical diagnosis; various scoring systems to aid treatment (PAS,    Alvarado score, etc.), CBC (leukocytosis), +/- imaging (US vs. CT)

Treatment: Surgical resection

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Pelvic Inflammatory Disease (PID):

Epidemiology: Sexually active females, younger age (15-25 yo), prior STIs, previous PID are all known risk factors; method of contraception also important (barrier is protective)

Pathophysiology: Two stages: Stage 1) acquisition of a vaginal or cervical infection (often STI); Stage 2) direct ascent of microorganism

Clinical Manifestations: Fever, nausea/vomiting, severe pelvic/abdominal pain, abnormal vaginal discharge (75% of cases), unanticipated vaginal bleeding, tenderness on pelvic exam (adnexal tenderness 95% sensitive)

Diagnosis: History/Physical, pregnancy test, CBC (leukocytosis), saline microscopy of vaginal fluid, ESR/CRP, STI testing, UA, +/- imaging

Treatment: Antibiotics against common organisms:

  • Regimen A: ceftriaxone, doxycycline, metronidazole
  • Regimen B: cefoxitin, doxycycline, metronidazole

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Ectopic Pregnancy:

Epidemiology: Increased incidence (4.5/1000 pregnancies in 1970 vs. 19.7/1000 in 1992) attributed to improved diagnostics; more common in women > 35 years old and non-white ethnic groups.

Pathophysiology: Any pregnancy in which the fertilized ovum implants outside the intrauterine cavity (>95% in the fallopian tubes)

Clinical Manifestations: Abdominal pain with spotting ~ 6-8 weeks after the last menstrual period; physical findings include slightly enlarged uterus, pelvic pain with movement of the cervix, and palpable adnexal mass

Diagnosis: History/Physical, pregnancy test, +/- progesterone, US

Treatment: Depends on patient stability:

  1. Expectant management: 68-77% resolve without intervention
  2. Medical management: methotrexate
  3. Surgical resection: salpingectomy via laparotomy

Ovarian Torsion:

Epidemiology: 5th most common surgical emergency in females; primary risk factor is an ovarian mass (particularly >5cm) or pregnancy (20%), can occur at any age – but most common in early reproductive years (median age 28 years)

Pathophysiology: Ovary rotates around both the suspensory and utero-ovarian ligament; rotation results in compression of the ovarian vessels (vein before artery) leading to ovarian edema and eventually ischemia

Clinical Manifestations: Classic presentation: acute onset of moderate-severe pelvic pain (90%), often with nausea/vomiting (47-70%), in a women with an adnexal mass (86-95%); other symptoms include fever (2-20%) and abnormal vaginal bleeding (4%)

Diagnosis: History/Physical, pregnancy test, CBC, pelvic US with doppler

Treatment: Surgical evaluation with detorsion or resection

Yersina Enterocolitica:

Epidemiology: Most often due to consumption of raw or undercooked pork; young individuals more often (75% are 5-15 years old)

Pathophysiology: Following consumption, invasion and penetration occurs in the ileum (M cell) => multiplication in Peyer patches (underlying lymphoid tissue) => mesenteric lymph => node spread => localized infection => systemic infection (rare)

Clinical Manifestations: Fever, abdominal pain, and diarrhea ~ 4-6 days after exposure; pain often localized to the right-side of the abdomen (pseudoappendicitis)

Diagnosis: History/Physical, stool culture for yersinia

Treatment: Supportive care typicially; aminoglycosides and TMP-SMZ if severe

Pyelonephritis:

Definition:

  • Pyelonephritis is an infection of the upper urinary tract, specifically the renal parenchyma and renal pelvis
  • Cystitis refers to an infection of the lower urinary tract, specifically the bladder

Epidemiology:

  • Women > Men (11.7 vs 2.4 hospitalizations per 10,000 cases)
  • Men > Women (16.5 vs 7.3 deaths per 1000 cases)

 

PID Cystitis Pyelonephritis
Dysuria + + +
Discharge +
Abdominal Pain + + +
Fever + +
Frequency/Urgency + + +
CMT +
CVA +

Pathogenesis:

  • Most renal parenchymal infections result from bacterial ascent through the urethra and urinary bladder
  • In males – prostatitis and prostate hypertrophy (causing urethral obstruction) predispose to bacteriuria

Uncomplicated Pyelonephritis:

  1. Typical pathogen
  2. Immunocompetent patient
  3. Normal urinary anatomy/renal function

Treatment:

Outpatient:

  • Oral fluoroquinolone (i.e. ciprofloxacin)
  • Recommended given low resistance rates (1-3%), absorbed well from the GI tract, excellent kidney penetration
  • Other acceptable options for susceptible organisms include:
  1. Amoxicillin-clavulanate (preferred for pregnancy)
  2. Cephalosporin
  3. Trimethoprim-sulfamethoxazole

Inpatient:

  • IDSA recommends one of three IV therapies:
  1. Fluoroquinolone (i.e. ciprofloxacin)
  2. Aminoglycoside (i.e gentamycin) +/- ampicillin
  3. Extended-spectrum cephalosporin +/- aminoglycoside
  • 7-14 days is effective; but studies suggest that 5-7 is comparable to longer duration in terms of clinical and bacteriologic outcome
  • Therapy with appropriate empiric antibiotics should produce improvement within 48-72 hours; failure should additional testing for an alternative diagnosis

AM Report 11/08/16 Endocarditis

Risk factors for developing Infective Endocarditis 

-Recent dental/surgical procedure
-Prosthetic valve
-Valvular or congenital heart disease
-IVDU
-Indwelling IV catheter
-Immunosuppression

Signs and Symptoms of Endocarditis

-Fever (90 % of patients!)
-Murmur (85 % of patients)
-Petechiae (20-40 % of patients)
Splinter hemorrhages (~10-15 %)
Splenomegaly
Janeway lesions-Non-tender, erythematous MACULES on palms and soles
Osler nodes- tender, subcutaneous violaceous NODULES, usually on pads of finger and toes
Roth spots– exudative edematous hemorrhages in retina with pale centers

*Remember that peripheral findings are uncommon (<10 %) unless protracted and untreated bacteremia

Indications for surgical repair in endocarditis

-CHF (eg: worsening valvular involvement)
-Perivalvular extension (eg: abscess, development of AV block)
-Systemic embolism
-Prosthetic valve
-CVA
-Persistent sepsis
-Resistant organism (eg: Staph aureus, pseudomonas, fungus)
-Large vegetation (>10-15 mm)

Common organisms implicated in Endocarditis (not an exhaustive list) 

-HACEK organisms (found in oral-pharyngeal region, Haemophilus, Aggregatibacter (previously Actinobacillus), Cardiobacterium, Eikenella, Kingella)
-Staph aureus (most common cause in IVDU)
-Coagulase negative staph
-Strep Gallolyticus (formerly known as Strep Bovis)
-Viridans Strep
-Enterococci

 

AM Report 11/9/16: Heparin-Induced Thrombocytopenia

Remember the different types of HIT:

 

Type 1 Type 2
Mechanism Direct effect of heparin (non-immune) Immune (Ab)-mediated IgG against platlet factor 4-heparin complex
Incidence 10-20% 1-3% with UFH; 0-0.8% with LMWH

 

Onset After 1-4 day of heparin therapy

 

After 4-10 day; but can occur <24 h if prior exposure w/in 100 days (persistent Ab). Postop highest risk. Can occur after heparin d/c’d

 

Platelet nadir >100,000/μL

 

~60,000/μL, ê 50%

 

Sequelae None Thrombotic events (HITT) in 30-50%; rare hemorrhagic complications

 

Management Observe Cessation of heparin, alternative non-heparin anticoagulation to prevent thrombosis

 

Pathophysiology:

5

  1. Autoantibodies (IgG) are formed to platelet factor 4 (PF4) complexed with heparin
  2. Platelet Fc receptors bind the antibody-heparin-PF4 immune complex
  • Thrombocytopenia occurs by two mechanisms:

1) Platelet removal by splenic macrophages
2) Platelet consumption due to thrombus formation

Clinical Variability:

  • 10 times higher incidence with UFH compared with LMWH
  • A metaanalysis of 15 studies (>7000 patients) that evaluated the risk of HIT with prophylactic UFH vs LWM found the following absolute risks of developing HIT
  • UFH – 2.6% (95% CI 1.5 – 3.8%)
  • LMH – 0.2 % (95% CI 0.1 – 0.4%)
  • Surgical > Medical patients; Incidence is particularly high after orthopedic surgery

4.jpg

Risk Factors:

  • There is no dose of heparin that is too low to cause HIT! Patients have developed HIT after exposure to as little as 250 U flush.
  • Female sex appears to be at a higher risk for unclear reasons – this was based on 7 trials comparing UFH vs LWH found approximately twice the risk.

Clinical Manifestations:

  • Thrombocytopenia (<150,000/microL ~ 85-90%)
  • Platelet drop of >50% is typical with mean nadir of 60,000/microL and RARELY <20,000/microL
  • Typical onset is 4-10 days after heparin therapy
  • Patients with exposure to heparin in the previous 100 days can develop a early onset (<24 hours) HIT
  • Thrombosis occurs in up to 50% of HIT patients (venous > arterial); presenting finding in up to 25%
  • Thrombotic sequelae – skin necrosis, limb gangrene, organ ischemia/infarction

4T Score:

4-1

  • A total score <4 points has a very high negative predictive value (97-99%); additional testing is not necessary

Assuming an intermediate/high risk score – what other labs can aid in the diagnosis:

  • Anti-PF4 heparin antibodies – excellent NPV (98-99%), but low PPV due to presence of clinically insignificant antibodies (IgM, IgA)
  • Our lab restricts the antibodies to only IgG – which increases the specificity
  • Also provides an optical density (magnitude of anti-PF4-heparin reactivity) ~ greater activity (>2.0) correlates to a greater likelihood of HIT
  • Serotonin-release assay – functional assay that measures heparin-dependent platelet activation; a negative result rules out HIT

Treatment:

Step 1: Immediate cessation of heparin

Step 2: : Initiation of an alternative anticoagulant at a therapeutic dose.

  • Vitamin K antagonists should NOT be given until HIT has resolved (i.e. platelets > 150,000 for >2 days) because they increase the risk of venous limb gangrene/limb loss by decreasing levels of protein C.
  • Argatroban (direct thrombin inhibitor) is the only currently FDA approved medication in the US.  Danaparoid (anti-factor Xa) is approved in Canada, EU, and Australia.  Other options include: Lepirudin and Bivalrudin.

AM Report 11/7/16: Primary Polydipsia

Remember to check plasma osmolality first!

1

Next evaluate volume status!

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If a patient is Euvolemic – evaluate urine osmolality and sodium

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Practical approach to hyponatremia:

1.What is the normal/abnormal physiology?

2.Is it “true” hypo-osmolar hyponatremia?

  • Measure plasma osmolality

3.What is the volume and ADH status?

  • Urine Na and Urine Osmolality

4.Is it symptomatic?

5.What is my treatment?

  • Depends on volume status, ADH status, and +/- symptoms
  • Determine goal of correction
  • Avoid overcorrection

AM report 11/01/16 HOCM

Before considering HOCM, think about secondary causes of hypertrophic cardiomyopathy

-HTN
-Aortic Stenosis

Disease manifestations of Hypertrophic Cardiomyopathy

-LV outflow tract obstruction due to thickened septum (see picture below)
-Diastolic dysfunction
-Myocardial ischemia
-Mitral regurgitation

hocm.jpg


Clinical symptoms of HOCM

–Heart Failure (90 % present with DOE), due to LVOT, diastolic dysfunction, and MR
–Chest pain
–Arrhythmias-SVT and VT-risk of sudden cardiac death!
–Syncope

How to make the diagnosis? 

Start with an EKG!
-Look for severe LVH and biatrial enlargement, can suggest HOCM. Due to asymmetrical hypertrophy, can see deep Q waves in the lateral and inferior leads.

What do you see in this EKG of our patient who was found to have a new diagnosis of HOCM? See below for the answer

ekgprint
Severe LVH. Biatrial enlargement, deep T wave inversions throughout

Echocardiogram-see unexplained LV wall thickness >15 m (makes diagnosis), commonly asymmetric septal hypertrophy. Can also see SAM (systolic anterior motion of mitral valve, worsening obstruction), and LVOT.

Further workup

Ambulatory EKG monitoring:  24-48hr Holter to evaluate for arrhythmias
Exercise stress test-Risk stratification, GXT preferred. Evaluate degree of LVOT if not seen on echocardiogram
Cardiac MRI-risk stratification due to better visualization than TTE
-Note that genetic testing is NOT routinely done due to 11 genes, and >1500 mutations responsible, but can be considered as Autosomal Dominant inheritance.
Cardiac catheterization not routinely done unless high suspicion of ischemia

Medical treatment

-LOWER heart rate and DECREASE inotropy
-3 classes of medications commonly used
BETA BLOCKERS (first line)
Nondihydropyridine CCB (commonly Verapamil)
Disopyramide

-Classes of medications to AVOID

Diuretics-reduction in preload can worsen LVOT (don’t let them become hypovolemic!)
Vasodilators– decreased peripheral resistance can increase LVOT obstruction
–Positive Inotropes (eg: Dobutamine)

Non-pharmacologic therapies

1)Activity restriction-avoid high intensity exercise, need to be counseled on this as HOCM is the number one cause of sudden cardiac death in those under age 30!
2)Alcohol septal ablation
3)Surgical myomectomy

Who needs to get an AICD?

Only if you are HIGH risk based on risk stratification


-Highest risk if history of prior sudden cardiac arrest or sustained ventricular arrhythmias

Other high risk features include:
-Family History  of SCD
-Syncope
-NSVT
-Massive LVH>30 mm

Not everyone needs an AICD, eg: if asymptomatic and negative family history!