08/30/16 AM report: Thrombocytopenia

Think about thrombocytopenia in three broad categories after ruling out pseudothrombocytopenia

Pseudothrombocytopenia (low platelet count due to clumping in EDTA tube, repeat with heparin or citrate top to confirm)

Underproduction (anything in the BM that prevents production, usually affects other lines as well)

eg: marrow failure (aplastic anemia), nutritional deficiency (B12/folate/copper)
eg:marrow invasion-leukemia, tumor, fibrosis, granulomatous diseases like sarcoidosis)
eg:marrow injury-drugs (long list), radiation, infection (Hep C, viral, HIV), sepsis
eg:congenital (Wiskott Aldrich, Bernard Soulier)

-Splenic sequestration (anything that can cause splenomegaly. eg: cirrhosis)

-Peripheral destruction (can be broken up into immune mediated and non-immune mediated)

Etiologies of thrombocytopenias that are life-threatening and can cause thromboses in addition to bleeding-does your patient have one of these?

HITT-need to discontinue heparin and treat with non-heparin anticoagulant (eg: direct thrombin inhibitor, Argatroban), can cause arterial and venous thromboses
APLS– associated with both arterial and venous thromboses
DIC-risk of bleeding and thromboses (usually venous)
-HUS-TTP-can be life-threatening if plasmapheresis is not initiated

ITP

-Acquired thrombocytopenia due to auto-antibodies against platelet antigens
-Usually ISOLATED thrombocytopenia without anemia or leukopenia
-Can be Primary or Secondary

Secondary etiologies: HIV, Hep B,C, CLL, SLE, APLS, H Pylori, thyroid disease

Treatment: 

1)Asymptomatic and platelet count >30-40k: no treatment!
2)Symptomatic: Glucocorticoids/IVIG
3)Refractory: Rituximab, TPO agonist (Eltromabag, Romiplostim), splenectomy

Comparing ITP vs. TTP vs. DIC (http://emedicine.medscape.com/article/206598-overview)

ITP vs DIC vs TTP

8/29/16 AM Report: Hyperthyroidism

Recognize the physical exam findings of hyperthyroidism! 

Skin: warm moist skin, pretibial myxedema(Graves disease), thyroid acropachy, clubbing (Graves)
Eyes: Lid lag, stare, Proptosis (Graves disease), extra-ocular impairment (Graves disease)
CV: arrhythmias (sinus tachycardia, atrial fibrillation), high output CHF
Neuro: fine tremor, hyperreflexia
Psych: anxiety, agitation, psychosis, depression, insomnia, mania
Thyroid: diffuse thyromegaly, thyroid bruit (specific for Graves)

See the Stanford 25 website on how to do a thyroid exam 

High radioactive iodine uptake on RAIU scan in hyperthyroidism (de novo synthesis of thyroid hormone) 

1)Graves disease-can also diagnose with TSI-high sensitivity/specificity
2)Toxic adenoma
3)Multinodular Toxic Goiter
4)Iodine deficiency (rare in the USA)

Low radioactive iodine uptake on RAIU scan in hyperthyroidism (inflammation and destruction of thyroid tissue with release of pre-formed hormone OR extra-thyroidal source of thyroid hormone)

1)Thyroiditis (subacute granulomatous thyroiditis (De Quervains), painless, post-partum, suppurative/infectious thyroiditis)
2)Exogenous thyroid hormone administration
3)Struma Ovarii
4)Drug induced (eg: Amiodarone)
5)IV contrast load

Treatment

-Methimazole and beta blockers (eg:Propranolol) for hyper-adrenergic symptoms
-AVOID radio-iodine ablation if Graves’ ophthalmopathy, as can worsen eye involvement but
-Monitor for risk of agranulocytosis and hepatotoxicity with Methimazole!

See picture below for symptoms of hyperthyroidism! (copyright Nursing Education Consultants Inc) *Note that hyperdefecation commonly occurs, not diarrhea.

hyperthyroidism

 

8/25/16 AM Report – VZV Encephalitis

CSF Study Interpretation:

CSF Studies:
Normal Bacterial Meningitis Viral Meningitis Fungal/TB
Opening Pressure (cm H2O) < 15 ↑↑ Normal/mild ↑ Variable (very elevated with crypto)
Protein (mg/dL) 15-45 Normal/mild ↑
Glucose (mg/dL) 40-70 Normal
WBC 0-8 ↑↑ (>1000) ↑ (5-300)
WBC differential Even >80% PMNs >50% Lymphs, <20% PMNs 50-80% Lymphs
Gram Stain Normal 60-90 % + N/A 37-87% AFB +

CT Before LP:
1) Altered Mental Status / Fecal Deficits
2) Immunocompromised
3) History of CNS disease – mass lesion, stroke, etc.
4) Seizure within 1 week of presentation
5) Papilledema

Bad causes of headache to always think about:
– Meningitis (or other CNS infection)
– Tumor/Space occupying lesion
– SAH
– Temporal arteritis

Headaches: POUNDPulsatile, One day, Unilateral, Nausea, Disabling
Migraine:
Epi: 3x more common in adult females; peaks in the 5th decade of life
S/S: unilateral, throbbing headache, +/- photophobia/phonophobi/nausea

Tension-Type Headache
:
Epi: stress/sleep disruption are common triggers
S/S: bilateral, steady, mild-moderate discomfort

Cluster Headache:
Epi: male sex/tobacco use are risk factors; typically occurs within a few hours of falling asleep
S/S: periorbital/temporal intense pain usually ipsilateral; can develop autonomic features such as ptosis, lacrimation, conjunctival injection, and rhinorrhea

Clinical Manifestations of VZV:
Rash: erythematous papules progressing to grouped vesicles; usually limited to one dermatome, but can affect 2-3 neighboring dermatomes. Thoracic/Lumbar dermatomes are most commonly involved.
Acute neuritis: most common symptom; 75% have prodrome of pain – usually described as “burning, throbbing, stabbing.”

HZ Ophthalmicus:
serious, sight-threatening condition caused by VZV reaction within trigeminal ganglion. Usually preceded by prodrome of headache, malaise, fever.
2
Hutchinson’s Sign:
vesicles on the tip of the nose – associated with HZ opthalmicus.
1
Ramsey-Hunt Syndrome: major otologic complication of VZV reactivation.
Triad (typicially) 1) Ipisilateral facial paralysis
2) Ear pain
3) Vesicles in auditory canal

8/23/16 AM Report – Wernicke’s Encephalitis

Wernicke’s Encephalitis (WE) Triad:
1) Encephalopathy
2) Ataxia
3) Oculomotor dysfunction
* presence of all 3 symptoms is not needed in order to make the clinical diagnosis; only approximately 10% of patients will display all 3 symptoms.

Korsakoff Syndrome (additional 2 findings):
4) Selective anterograde/retrograde amnesia
5) Confabulation

WE is an under-recognized disease with a prevalence of 0.4 – 2.8% in the general population and up to 12.5% in alcohol abusers.
WE is more common in men, but women are more susceptible to development.

Caine Criteria – proposed in 1997 (article below) – only need 2 of 4 for diagnosis
1) Dietary deficiency
2) Oculomotor dysfunction
3) Cerebellar dysfunction
4) AMS or mild memory impairment
* study of 106 autopsied alcoholics found that use of the Caine criteria from the standard WE triad increased the diagnostic sensitivity from 22% (classic triad) to 85% (Caine criteria).

Remember that WE can be associated with a number of conditions/diseases (not a compelte list):
– Chronic alcoholism
– Anorexia/dieting
– GI surgery (esp. bariatric)
– Dialysis
– Prolonged IV feeds without supplementation
– Sepsis (high catabolic state)

Pathophysiology – WE is due to thiamine (vitamin B1) deficiency. Remember to WE is a clinical diagnosis and treatment should be started early to prevent irreversible damage.  Response to therapy may be diagnostic.

No lab testing is needed for diagnosis!

Treatment:
Thiamine IV 500 mg TID Days 1-2
Thiamine IV 250 mg BID Days 3-5
Thiamine PO 100 mg daily, which should be continued until the patient is no longer at risk.

* Avoid glucose before thiamine if possible – can precipitate an episode of WE.

8/23/16 AM Report-Skeletal Tb

~10-35 % of extra-pulmonary Tb is skeletal Tb, most common form is Pott’s disease (Spondylitis)

Differential for malignancy related bone involvement

-Metastatic disease much more common than primary bone cancer
Mnemonic for cancers that  go to bone: BLT + Mayo and a Kosher Pickle

B=Breast
L=Lung
T=Thyroid
Mayo=Multiple Myeloma
Kosher=Kidney
Pickle=Prostate

Don’t forget about infections!
Infection (eg: staph aureus osteomyelitis),  histoplasmosis, coccidomycosis, Tb!

Extra-pulmonary Tb-it’s not just in the lungs!

Miliary Tb=clinical disease from hematogenous spread of Mycobacterium Tb, can spread to…

Lungs- (>50 % of patients with Miliary Tb)
-Lymphatic disease-Tb lymphadenitis
Bone and joint disease- Pott’s disease, skeletal Tb
-GI disease-TB enteritis, peritonitis or hepatic disease
CNS-Tb meningitis, tuberculoma
-Genitourinary, adrenal disease-renal papillary disease, adrenal insufficiency
-CV-pericarditis
Skin-Tb Cutis Miliaris

Tb can spread everywhere, make the diagnosis by biopsy and AFB stain & culture, treatment is with RIPE therapy 

MTB Blog

 

 

 

 

 

 

8/22/2016 AM Report – Euvolemic Hyponatremia

Step 1: Make sure its really hypotonic hyponatremia
Pseudohyponatremia (lab error)=HLD, multiple myeloma
Hypertonic hyponatremia=hyperglycemia, mannitol, IVIG etc.
Confirm with serum osmolarity if not sure (normal is 280-300)

 
Step 2: What is the volume status? Use the H&P!

 
History: CHF, nephrotic syndrome, cirrhosis, ask about poor PO intake, vomiting, diarrhea, excessive water intake, and diuretic use
Physical exam: Look at JVP, skin turgor, orthostasis, vital signs

Step 3: If euvolemic, next step is checking urine osm

If LOW <100, and low urine sodium, think of two things

Primary polydipsia (eg: psychiatric patient, marathon runner, or MDMA use)
Low solute diet (eg: tea & toast diet, beer potamania)

If HIGH, >100, and urine sodium >20

SIADH
Hypothyroidism
Adrenal insufficiency
Nausea/pain/stress

Treatment
Water restriction + close monitoring of urine output, urine osm, and serum sodium if primary polydipsia
If from low solute diet, replace solute in diet (eg: NS) but watch for rapid correction
Goal is no more than 6-8 meQ/24 hour period. Highest risk of osmotic demyelination syndrome if liver disease, malnutrition, hypokalemia, or alcohol use.

What if you over-correct?
Use D5W to slow down rate of increase by matching or higher rate than urine output
If unable to keep up with urine ouput, hit the brakes by giving Desmopressin but make sure patient is fluid restricted to avoid further hyponatremia

See article below on osmotic demyelination syndrome!
Osmotic Demyelination

8/18/2016 AM Report – Acute Chest Syndrome

Leading cause of death for patients with sickle cell disease!

Etiology

Vaso-occlusion within the pulmonary microvasculature and can be from triggers for vaso-occlusion (eg: infection, asthma, hypoventilation) or consequence of vaso-occlusion (from bone marrow and fat embolism)

Diagnosis
New radiographic consolidation AND at least one of the following
Temperature ≥38.5°C
>2 percent decrease in SpO2 (O2 saturation) from steady state at RA
PaO2 <60 mmHg
Tachypnea (per age-adjusted normal)
Intercostal retractions, nasal flaring, or use of accessory muscles of respiration
Chest pain
Cough
Wheezing
Râles

DDX

Acute Coronary Syndrome vs. Pneumonia vs. PE most common differential diagnoses.

*Note that PE can be in-situ thrombosis OR thrombo-embolic from lower extremities.

Treatment

Fluid management (avoid over-resuscitation, use hypotonic fluids)
Pain control
Antibiotics to cover atypical and CAP (usually cefotaxime/azithromycin or CTX/azithromycin)
VTE prophylaxis (high risk for VTE!)
Supplemental O2 and incentive spirometry (to prevent atelectasis)
If refractory, simple transfusion to increase hemoglobin to 10 or exchange transfusion for severe cases to achieve Hemoglobin S <30 % and goal hemoglobin of 10

Prevention of ACS
Hydroxyurea (not for acute episodes)
Chronic transfusion therapy (only if refractory to above)