Today we discussed a case of malignant pleural effusion causing complete opacification of a hemithorax. We learned the framework for subacute-chronic dyspnea, discussed the physical exam finding of clubbing, reviewed Light’s Criteria and discussed transudates and exudates. Here is a recap:
Subacute-Chronic Dyspnea DDx:
- Pulmonary (malignancy falls into all of these categories)
- Foreign body
- AVMs (HPS can cause these)
- Valvular disease
- Constrictive pericarditis
- Reduced PiO2
- compensation for metabolic acidosis
DDx for Clubbing:
- 80% with underlying respiratory disorders
- 10-15% with miscellaneous disorders
- Congenital cyanotic heart disease, liver cirrhosis, chronic diarrhea, subacute endocarditis
- 5-10% hereditary or idiopathic clubbing
Lights Criteria and Pleural Effusions (see this previous blog post for an excellent review)
DDx For Complete Opacification of a Hemithorax
- Trachea pulled toward opacified side
- Total lung collapse
- Pulmonary agenesis
- Pulmonary hypoplasia
- Trachea pushed away from the opacified side
- Pleural effusion
- Diaphragmatic hernia
- Large pulmonary mass
- Trachea remains central in position
- ARDS/pulmonary edema
- Pleural mass
- Chest wall mass
Today’s case was a middle-aged man with a history of stage 4 pancreatic adenocarcinoma who presented with somnolence and severe thrombocytopenia.
TTP should be suspected in any patient with thrombocytopenia and microangiopathic hemolytic anemia (MAHA) with schistocytes on peripheral blood smear. The classic pentad of fever, anemia, thrombocytopenia, renal failure, and neurological findings only occurs in 5% of TTP patients so a high index of suspicion is required for prompt treatment. GI symptoms, which are not included in the classic pentad of TTP, are relatively common so we suggest the following mnemonic.
Fever (10% of patients)
Involvement of skin (purpura)
Today’s case was a young man with alcohol use disorder who presented with delirium tremens refractory to high dose benzodiazepines and severe anion gap metabolic acidosis.
In the differential diagnosis for hyperthermia, tachycardia, and hypertension in a patient with alcohol use disorder and psychiatric comorbidities, it is essential to consider serotonin syndrome and neuroleptic malignant syndrome in your differential.
||Gradual, days to weeks
||72-96h after last drink
||Hyperthermia, tachycardia, labile or high BP
||Hyperthermia, tachycardia, hypertension
||Hyperthermia, tachycardia, hypertension
||Muscle rigidity (lead pipe), hyporeflexia
|Tremor, myoclonus, oculoclonus
||Days to weeks
The differential diagnosis for anion gap metabolic acidosis in an alcoholic patient is also wide, including alcoholic ketoacidosis, type A lactic acidosis from concurrent shock due to severe alcoholic pancreatitis, hepatitis, or aspiration pneumonia among other infections, type B lactic acidosis from ethanol itself, or coingestion of other toxic alcohols such as methanol or ethylene glycol.
It is important to rule out toxic coingestion in all patients with alcohol use disorder, altered mental status, and severe anion gap metabolic acidosis. Do this by calculating your serum osmolar gap with a formula that includes ethanol.
Serum osm= 2Na + BUN/2.8 + glucose/18 + ethanol/4.7
If the osmolar gap >10, coingestion should be high on your differential.
This morning we presented a case of SVC syndrome with complete thrombotic occlusion.
- What is it?
- Obstruction of blood flow through the SVC
- What are the three mechanisms by which this can happen?
- Extrinsic Pressure
- How does the body compensate?
- Collateral veins develop to return blood to the heart
Causes of SVC Syndrome
- Facial and neck swelling
- Chest pain
- Respiratory symptoms
- Neurological manifestations such as head fullness, which may worsen by bending forward or lying own
- Headaches, confusion, audiovisual disturbances
- Cerebral edema can be fatal
- Arm swelling
- Onset of symptoms depends on whether collaterals had a chance to form
- May see distended chest wall veins
- Pemberton’s sign may be positive
- initially discovered in the context of a goiter, it can also be useful to identify other causes of SVC obstruction
- have the patient raise their arms for two minutes and watch for increasing facial plethora (swelling and redness)
- Depends on urgency. If emergent, ABCs then straight to endovascular management with pharmacologic thrombolysis/balloon angioplasty/etc +/- stenting
- If non-emergent, can obtain imaging and biopsy and plan treatment course with chemotherapy or radiation
Lastly, check out Radiopedia! It’s a great learning tool and really fun too.
Today’s case was a middle-aged male with a history of untreated CML who presented with gum bleeding, hypoxia, and altered mental status, found to have accelerated phase CML, leukostasis, and tumor lysis syndrome.
Today we discussed an interesting case of acute encephalopathy due to hypercalcemia of malignancy due to bone metastases.
We first reviewed the importance of maintaining a broad differential for acute encephalopathy/delirium/acute confusional state/
We reviewed the following framework:
Neurologic / Toxic / Metabolic / Infectious / Other.
We then reviewed the differential for hypercalcemia. For those of you interested, please check out this awesome review video by Dr. Strong:
Our patient had hypercalcemia of malignancy and the following patients were made:
- It is the most common cause of hypercalcemia in inpatients
- The most commonly associated malignancies are breast, lung, multiple myeloma, and renal
- There are three major mechanisms for hypercalcemia of malignancy
- Secretion of PTHrP – 80% of malignancy related hyperCa
- Osteolytic Metastases – ~20% of cases
- Increased 1,25-OH-Vitamin D (calcitriol) 2/2 to increased 1-alpha-hydroxylase activity from activated macrophages in lymphomatous (and also granulomatous) tissue
- We reviewed the PTH-based algorithm and determined that it was a PTH-independent process (PTH low or low-normal) and then used the PTHrP, calcidiol and calcitriol to guide to the correct diagnosis which was confirmed by MRI and bone scan
Finally, here is a way to distinguish between malignancy related hypercalcemia and primary hyperparathyroidism (most common cause in outpatients & higher co-occurrence in patients with malignancy)
For treatment options, please see the following blog post for more details!