Complications of Diverticulitis… a pyogenic liver abscess!



  • Mean age of diagnosis 63 years old, but 16% of cases occur <age 45
  • Most common symptom is abdominal pain: 95% LLQ pain, 5% is RLQ pain (more common in Asian patients)
    • 10-15% of diverticulitis patients have dysuria, urgency, or frequency
  • In an otherwise healthy patients under the age of 70, uncomplicated diverticulitis without sepsis, significant leukocytosis, diffuse peritoneal signs, or fever >102.5 can be treated outpatient as long as the patient has access to close follow-up (3 days)
    • If symptoms and infectious markers have not improved in 3 days, abscess should be suspected and patient should be admitted and reimaged
  • Outpatient treatment of diverticulitis:
    • Antibiotics: Cipro and flagyl first line
    • No evidence for dietary restrictions, but most providers recommend clear liquid diet until symptoms improve
    • Colonoscopy 6-8w after symptoms resolved to screen for colorectal cancer
    • Prevention of recurrences:
      • High-fiber diet
      • No evidence for avoidance of nuts, seeds, or corn as was previously thought
  • Complications of acute diverticulitis: abscess, perforation, obstruction, and fistula (usually colovesicular)

Pyogenic Liver Abscess:

  • usually polymicrobial
    • EColi most common in Western world
    • Klebsiella most common in Asia (beware of hypermucoid variant)
    • Strep milleri group is common (anginosus, constellatus, intermedius)
    • Staph and strep pyogenes can occur after procedures such as embolization
  • Most common symptoms is fever 90%
    • Abdominal pain 50-75%
    • N/v, anorexia, weight loss, malaise
  • LFTs are no necessary elevated
  • Mainstays of treatment are percutaneous drainage vs. surgical drainage and prolonged course of antibiotics (4-6 weeks)

Malignant Pleural Effusion And White-Out!

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)
    • Airway
      • bronchitis
      • COPD
      • Asthma
      • Bronchiectasis
      • Foreign body
    • Parenchyma
      • PNA
      • edema
      • atelectasis
      • ILD
    • Vasculature
      • PE
      • pHTN
      • AVMs (HPS can cause these)
    • Pleura
      • Pleural effusion
      • PTX
  • Cardiac
    • Arrhythmia
    • Ischemia
    • Valvular disease
    • Tamponade
    • Constrictive pericarditis
    • Myocarditis
  • Other
    • Anxiety
    • Anemia
    • Reduced PiO2
    • Hypoventilation
    • compensation for metabolic acidosis
    • pregnancy
    • Thyrotoxicosis

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
    • Pneumonectomy
    • 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
  • Consolidation
  • ARDS/pulmonary edema
  • Pleural mass
  • Chest wall mass

Thrombotic Thrombocytopenic Purpura

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)


Renal involvement


Involvement of skin (purpura)

Neurological symptoms

GI distress

Refractory Delirium Tremens and Anion Gap Metabolic Acidosis

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.

  NMS Serotonin Syndrome DTs
Onset Gradual, days to weeks <24h 72-96h after last drink
Vital signs Hyperthermia, tachycardia, labile or high BP Hyperthermia, tachycardia, hypertension Hyperthermia, tachycardia, hypertension
Neuromuscular Muscle rigidity (lead pipe), hyporeflexia


Tremor, myoclonus, oculoclonus Tremor
Reflexes Hyporeflexia Hyperreflexia Hyperreflexia
Pupils Normal Mydriasis (dilated) Mydriasis (dilated)
Causative agent Dopamine antagonist Serotonin agonists Alcohol cessation
Treatment bromocriptine Benzos, cyproheptadine Benzos
Resolution Days to weeks <24h Variable

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.

SVC Syndrome with Complete Thrombotic Occlusion

This morning we presented a case of SVC syndrome with complete thrombotic occlusion.

SVC 101

  • What is it?
    • Obstruction of blood flow through the SVC
  • What are the three mechanisms by which this can happen?
    • Thrombosis
    • Invasion
    • Extrinsic Pressure
  • How does the body compensate?
    • Collateral veins develop to return blood to the heart

Causes of SVC Syndrome


SVC Symptoms

  • 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

Physical Examination

  • 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)

Treatment Options

  • 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.

Hypercalcemia of Malignancy


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/AMS.

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!