Thanks to our excellent ICU team for presenting a fascinating case of a 70M who had an lumbar drain after spinal surgery who develop abdominal pain and AMS raising concern for ACS and low CSF pressure.
- While ST elevation in aVR does not technically meet STEMI criteria, it can provide key information about apical ischemia and is a marker of poor prognosis in ACS.
- ST elevations in two contiguous leads raises concern for total occlusion of the corresponding coronary vasculature. Other EKG manifestations of total occlusion are rare but include: (1) Wellen’s EKG (2) new LBBB and (3) De Winter’s EKG – see below
- Suspect intracranial hypotension in patients who present with orthostatic headaches. This is a rare disease than occurs due spontaneous CSF leak or excessive removal of CSF in patients with a lumbar drain.
aVR in ACS
- In patients diagnosed with ACS, ST elevation in aVR does not meet true “STEMI” criteria, but
- Strongly predicts proximal LAD occlusion
- ST elevation in aVR > ST elevation in V1 suggests acute left main occlusion
- In patients with inferior STEMI, ST depressions in aVR suggests left circumflex infarction or large RCA infarction.
ST elevations in two contiguous leads raises concern for acute total occlusion of the corresponding coronary artery. While this is the most common EKG pattern of total occlusion, several other “STEMI equivalent” can also occur.
- Wellen’s T waves (https://lifeinthefastlane.com/ecg-library/wellens-syndrome/)
- Deep, symmetric (Type B, 75%) or Biphasic (+ then -, 25%) V2-3 (may extend to V1-6)
- Isoelectric or minimally-elevated ST segment (< 1mm)
- No precordial Q waves
- Preserved precordial R wave progressions
- De Winter’s pattern (https://lifeinthefastlane.com/ecg-library/de-winters-t-waves)
- Concave ST depressions into tall, symmetric T waves in the anterior precordial leads
- ST depressions in the anterior leads + tall R waves
- Get posterior EKG looking for posterior STEMI
- LBBB in the setting of acute chest pain
- Subtle STEMI
- 1/20 of all acute coronary occlusions do not meet criteria for STEMI, instead cause 0.7 – 0.9 mm ST elevations termed “subtle-STEMI”
- In this setting, look for reciprocal depressions
- The RCA is usually involved
- ST depressions in inferior leads —> scrutinize the high lateral leads (I and aVL) for subtle ST elevations
- ST elevations in inferior leads, scrutinize, the high lateral leads to ST depressions (>0.5 mm)
Subtle STEMI: Wei, Margaret, Daniel R. Sanchez, and Ivan Rokos. “Nondiagnostic ST Elevations With Chest Pain: The Subtle STEMI.” JAMA Internal Medicine177.4 (2017): 577-578.
Thanks to Anne Rohlfing for presenting an interesting case of a 66M with severe COPD who presented with dyspnea found to have likely CAP and severe hyponatremia
- The FEV1% classifies disease severity in patients with COPD. Other supportive information includes – (1) need for home O2 (2) frequency of exacerbations (3) history of intubation (4) medications (e.g rofllumilast – only approved for severe COPD)
- A VBG is a less precise test than an ABG but is more convenient. Get a VBG when you need a sense of the pH and PCO2. An ABG is important when this information is critical to the management
- Consolidation on CXR usually represents an infection. In rare causes, mimickers of this can be considered by the nature of the fluid. See below for details.
VBG versus ABG
Where can a VBG be obtained from?
What numbers can be obtained?
- Categorize shock (only useful in central VBG)
- This number is not helpful as the majority of oxygen has been consumed in the capillary bed
Converting a VBG to an ABG
While there are some subtle differences between central and peripheral VBG’s, but as a general rule:
- pH – add 0.05 to VBG —> ABG
- CO2 – subtract 5mm to VBG —> ABG
- Central venous blood gases correlates much better with ABGs that peripheral VBGs
- Peripheral VBGs are even less reliable in
- Hypotensive patients
- Issues with technique
- Prolonged tourniquet application
- Delayed sample collection
- In these situations, the venous pH is more accurate than the pVCO2
Putting this together
- The ABG is the gold standard test for assessing pH, pCO2 and pO2
- While VBGs are less reliable, there are more convenient
- For most clinicians, convenience of VBGs outweighs their imprecision when a sense of the pH and acid base status is needed (e.g. non-severe COPD exacerbation, mild acidosis)
- Get an ABG where this information is critical to decision making (e.g intubation, severe acidosis/alkalosis)
Alveolar infiltrate on imaging
The vast majority of alveolar infiltrates ( = consolidation) represent bacterial, or viral, pneumonia. Mimickers of this clinical syndrome can be generated by considering the nature of the fluid –
- Complicated bacterial pneumonia – the radiologic abnormalities resolves in a delayed manner (~ 2 months) but failure to improve/recurrent alveolar infiltrates in the same distribution prompts consideration of (1) obstruction (malignancy) (2) immunodeficiency (HIV) or anatomic pulmonary pathology (bronchiectasis)
- In immunosuppressed patients broaden the infection DDX to consider (1) atypical bacterial infections (Tb, Nocardia) or fungi (PCP, Crypto, aspergillus)
- Cardiogenic pulmonary edema
- Unilateral pulmonary edema has been described in CHF – more so with mitral regurgitation
- Non-cardiogenic edema -> ARDS
- Bland pulmonary hemorrhage (e.g. as a complication anti-coagulantion)
- Inflammatory (vasculitis)
Sterile inflammation (cells without organisms)
- Interstitial lung disease
- Acute or chronic eosinophilic pneumonia
- Hypersensitivity pneumonitis
- Autoimmune pulmonary disease (scleroderma, dermatomyositis)
- Drug-induced pulmonary disease
- PD-1 inhibitors
- Radiation induced
- Inhalational injury
- Infiltrating adenocarcinoma
- Lymphangitic spread of tumor
- Pulmonary alveolar proteinosis
Thanks to our ICU team for presenting an interesting case of a 74M with esophageal CA c/b low grade GIB who presented with ACS and found to have triple vessel disease
- Peripheral arterial disease commonly co-occurs with CAD –> check pulses in your patients presenting with chest pain.
- The complications of a femoral access include pseudoaneurysm, AVM and RP hematoma. Cholesterol embolization syndrome is a delayed complication.
- In patients with CAD, be more aggressive with controlling the sympathetic surge that accompanies alcohol withdrawal.
Check out this graph about the manifestations of EtOH withdrawal – courtesy of Anna Parks!
- Patients can develop signs of withdrawal as early as 6 hours after their last drink
- Initial symptoms and signs are that of sympathetic hyperactivity
- Tremor, anxiety, tachycardia and tachypnea
- Delirium tremors usually develops 72 hours after last drink and is characterized by
- Altered sensorium
- This is the distinguished feature of DTs
- Increased autonomic dysfunction
- Risk increases after 24 hours
- Most seizures are generalized tonic clonic and rarely last > 3 min
- Rule out other causes of seizure that occur more commonly in patient with alcohol use disorder
- Subdural hemorrhage
- Nutritional deficiencies (pyroxidine > thiamine in terms of seizure risk)
- Traumatic encephalopathy
- This can create a nidus for seizure activity independent of EtOH use
There is an increasing number of treatment options for EtOH withdrawal. It is helpful to divide these options into GABAergic agents versus GABA independent drugs.
- The primary reason to do so is because GABA independent agents do not protect from EtOH withdrawal seizures
- First line option for most patients
- Phenobarbital is an increasingly utilized option especially for patients being dc’d from the ED
- Use this in patients who are intubated and experiencing EtOH withdrawal
GABA independent agents
- Central acting alpha blocker that reduces the CNS sympathetic outflow
- This is a great adjunct to one of the agents above.
- Similar mechanism to above
- Used less frequently
- Increasingly used and incorporated in CIWA protocols specifically for agitation
- Helps reduce BzD use
- Caution with QTc prolongation
- Gabapentin and Carbamazepine are other less frequently used adjuncts to reduce BzD requirement.
Thanks to Jackie and Bennett for presenting an very interesting case of a 77M with history remote colon CA w/ ileostomy who presents with fatigue superimposed on chronic weight loss found to have hyponatremia c/b rapid correction.
- Check out Christy’s awesome past re: weight loss at https://ucsfmed.wordpress.com/category/ambulatory/
- LT’s DDx for unclear weight loss thats persists > 1 year without a DX includes endocrinopathy (diabetes, addison’s disease) and two chronic disease (whipple’s disease and sarcoidosis). However, co-morbid psychiatric disease and mesenteric ischemia are the two most likely causes.
- Osmotic demyelination syndrome (formerly central pontine myelinolysis) presents in a delayed manner – 2-3 days after the insult.
Hyponatremia – Approach
- Here is one approach to hyponatremia that is more dependent on the labs (serum osm, urine osm and urine sodium) than on the volume status
Hyponatremia – overcorrection
While severe hyponatremia can be life threatening, usually the patient is sickest at presentation and will only get better with therapy. Adverse patient outcomes emerge from rapid overcorrection of hyponatremia
Why is the this a problem?
The rapid increase in serum osmolarity with correction of hyponatremia results in diffusion of water from the cells into the serum. This is most problematic in the brain and leads to the osmotic demyelination syndrome
Osmotic Demyelination syndrome
- Formerly known as central pontine myelinolysis, but the name changed after recognition of other neurologic syndromes from osmotic demyelination outside the brainstem (diffuse white matter disease, most commonly)
- This most commonly occurs as an iatrogenic complication with rapid correction of hyponatremia
- The rate of rise in the Na is most predictive. Other risk factors include
- Severity of hyponatremia (low risk if Na > 120; the lower the initial Na the higher the risk)
- There is a wide range of neurologic deficits depending on the primary lesions
- Brainstem (pontine) disease is the most morbid
- Symptoms are usually delayed by two – 6 days
- MRI can support the diagnosis but the clinical context (rapid rise in osm) is critical.
What is the recommended rate of correction?
- In acute hyponatremia (< 24 hours), correction can be made over 24h
- Only assume acute hyponatremia when there is a documented dropped in the Na over this period of time
- Treat everyone else as chronic
- Chronic hyponatremia
- Goal is a rising in serum Na by 6-8mEq in 24hours
- In symptomatic hyponatremia requiring 3% saline, a large portion of this correction can be done in the first few hours.
Are there patients who are particularly prone to have rapid corrections in their sodium?
- Rapid termination of the stimulus that lead to ADH
- Rapid correction of hypovolemia
- Discontinuation of a medication causing SIADH (SSRIs)
- Spontaneous resolution of a cause of SIADH (nausea, pain)
- Receipt of hypertonic solution
- Sodium Bicarbonate
- Tube feeds (without free water bolus)
How is rapid correction of hyponatremia managed?
- In these patients have a low threshold to consult renal
- Goal – reduce serum Na by 1mEq/hr
- D5W 6mEq/kg infused over 2 hours
- dDAVP 2mcg IV/Subq every 6 hours
- The role of DDAVP is to “lock” renal free water excretion to ensure that the free water given (D5W) is retained
- Measure serum Na q2h initially and adjust the dose of the D5W accordingly
Thanks to our awesome ICU crew for presenting a fascinating case of a 56M with psoriasis on a TNF blocker who presented with confusion, diarrhea found to have multifocal pneumonia and ultimately diagnosed with legionella!
- Although TNF alpha inhibitors are classically associated with increased susceptibility to opportunistic infections (Tb and Histoplasmosis most commonly), more importantly it leads to more severe and atypical presentations of more common illnesses.
- The lateral CXR is a great addition to the AP/PA film and can see
- Retrosternal pathology
- Retrocardiac disease
- Pathology hidden behind the diaphragms
- While severe community acquired pneumonia is usually due to a severe manifestation of a common cause of CAP, but consideration of less common causes is important.
Severe community acquired pneumonia
- While CAP is one of the leading causes of death worldwide, the vast majority of infections have a benign clinical course (most CAP is treated as an outpatient).
- Severe CAP (requiring ICU) admission is usually due to a severe manifestation of a common organism. However, it’s important to broaden the DDx in these patients.
- Frequently, historical clues (exposures), radiographic pattern of disease and extra-pulmonary manifestations will help limit this broad DDx.
- A water borne (man-made water sources) fastidious gram negative rod
- There are over 58 subspecies
- L. Pneumonphilia type 1 causes the majority of infections
- It’s best to file legionella as a multi-system illness with primary pulmonary manifestations
- Legionella can affect any host, but these sub-populations are at high risk
- M > F
- Age > 50
- 25% of patients have a recent travel history
- 62% of cases occur in the summer/autumn
- A less common form of legionella that results in an influenza-like upper respiratory illness
- The true pathogenesis (infections versus allergic) is not clear
- The vast majority of patients are young, healthy, and improve without antimicrobials
- As a result, the majority of patients remained undiagnosed.
- A multi-system disease with primary pulmonary manifestations
- General features
- Incubation period: 2-14 days
- Prodrome of influenza like features is common
- Like influenza, a high fever is characteristic
- Relative bradycardia is occasionally found
- Pulmonary disease
- Lower respiratory tract disease develops in the majority of patients
- Unilobar infiltrate is the most common CXR manifestation
- Multifocal opacities can occur
- Nodular disease is more common in immunosuppressed patients
- Cavitary disease may also develop even in patients with appropriate Rx
- Extra-pulmonary disease
- Gastrointestinal disease
- Diarrhea is not an uncommon manifestation of any cause of CAP
- However, legionella is characterized by a particularly severe (bio-fire negative) diarrhea
- Other GI features
- Hepatitis (mild)
- Pancreatitis (mild)
- Neurologic disease
- A wide of neurologic symptoms are often present, ranging from headache to
- Focal neurologic changes
- Mild CK elevations are common
- Acute Kidney Injury
- ATN or AIN may be present.
- Laboratory clues (all non-specific but contribute to the clinical picture)
- AST,ALT, lipase, elevated CK as above
- Low phosphorous
- Leukocytosis with lymphopenia
- Ferritin > 2ULN
- In summary, suspect these diagnosis in a patient with pneumonia who has a high fever, prominent GI and neurologic symptoms.
- While many diagnostic tools are available (BAL, respiratory culture) the diagnostic test of choice is the urinary legionella antigen
- However, this is limited to L.Pneumophilia type 1 (the subspecies most strongly linked to severe clinical disease)
- Levofloxacin or azithromycin are the antibiotics of choice.
Thanks to Vaibhav for presenting a very interesting case of a 48M with no PMH who presented with dyspnea and found to have possible pulmonary sarcoidosis!
- An detailed exposure history is an important aspect in the diagnostic approach to ILD. Ask about smoking, dust exposure, animal protein (bird), fungal/bacterial elements and medications.
- An elevated DLCO is most commonly due to asthma. Other causes include pulmonary hemorrhage, a left–> right shunt or polycythemia.
- The most common PFT pattern of ILDs is restrictive lung disease. Some ILDs can also result in an obstructive pattern. These include sarcoidosis and hypersensitivity pneumonitis.
Approach to PFT interpretation
- PFTs are an important part of the work for a patient with pulmonary disease.
- As Goop reminded us, they have to be interpreted with caution as patient effort and tech expertise can have significant impact on the results.
- Flow volume loops are less vulnerable to these effects.
- Here’s an approach to interpreting PFTs from the AAFP
Approach to obstructive lung disease
- Asthma and COPD are the two most common obstructive lung diseases.
- In these diseases obstruction occurs at the level of the “middle to lower airways”.
- Bronchiectasis (from any cause) is another middle-lower airways disease that causes obstruction
- Airway obstruction in the central or distal airways is less common.
- A disease of distal airways characterized by gas trapping, bronchial wall thickening and centrilobular nodules
- It may be a distinct entity or associated with an ILD (see below)
- Suspect when there is obstructive lung disease with the above HRCT findings along with an absence of wheezing
- Acutely, this is commonly due to infections (RSV, mycoplasma)
- Chronic bronchiolitis is further divided into
- Obliterative bronchiolitis
- Fibrotic destruction of the distal airways
- Associated with lung transplant (>70% of patients) or stem cell transplant
- Respiratory bronchiolitis
- Foamy macrophages infiltrating the distal airways
- This is one of the smoking-related ILDs
- Granulomatous infiltration of the distal airways
- Sarcoidosis, IBD, hypersensitivity pneumonitis
- Follicular bronchiolitis
- Lymphoid tissue infiltrating the distal airways
- Associated with autoimmune diseases (RA > Sjogren’s)
- DLCO measures the diffusion of carbon monoxide across the alveolar-capillary interface
- Any process than reduces the # of alveoli-capillary interfaces (COPD, pulmonary hypertension) or increases the distance between alveoli and capillary (fibrosis from ILD) will reduce the DLCO.
- Asthma is the most common reason for an elevated DLCO (mechanism unknown)
- Any process than increases the intrathoracic blood volume
- Pulmonary hemorrhage
- Mild pulmonary edema
- A mild degree is one that leads to engorgement of the pulmonary vessels without extravasation into the interstitium
- Left –> right cardiac shunt
- Supine position
Thanks to Chuka for presenting an interesting case of a 21F with history of IDU, staph aureus endocarditis who p/w malaise and found to have acute liver injury, hypoglycemia and subsequently developed valvular cardiogenic shock
- Divide the hypoglycemia ddx into insulin mediated versus non-insulin mediated. This maps on to the not-sick (insulin mediated) versus sick (non-insulin mediated) approach.
- In a hypoglycemic patient, the absence of ketones on UA suggests an insulin mediated cause.
- An elevated SvO2 suggests impaired oxygen extraction. This is usually due to sepsis but also be due to arteriovenous shunting or mitochondrial toxicity syndromes.
*See Anna’s great post for more pearls about acute liver injury/failure/LFTs >1000: https://ucsfmed.wordpress.com/2017/07/18/va-morning-report-7-18-17-acute-liver-injury-and-aortic-dissection-deep-cuts/
Step 1: Is this true hypoglycemia?
- Before pursuing a work up of hypoglycemia ensure that Whipple’s triad has been met:
- Symptoms present
- Hypoglycemia present
- Symptoms resolve with correction of hypoglycemia
*This stems from the absence of a true cut off for hypoglycemia
- Consider the possibility of pseudo-hypoglycemia:
- Cool extremities
- Consumed in test tube from:
- Classify as insulin (or IGF) mediated versus non-insulin mediated
- Features that support an insulin-mediated process:
- Suppressed ketosis
- Symptoms of hypoglycemia predominate in insulin-mediated disease, other problems dominate in non insulin (e.g sepsis)
- Patients with insulin mediated hypoglycemia are otherwise well-appearing. Non-insulin mediated hypoglycemia occurs in patients who are otherwise sick.
- Insulin intake
- Insulin secretagogue intake
- Accidental sulfonylurea intake (or AKI in patient on sulfonylurea)
- Commonly laced in street drugs (Benzos most common)
- Octreotide may be therapeutic
- Non-insulomatous pancreatic hyperplasia
- Post-gastric bypass
- Hirata syndrome
- Sulfa drug induces insulins antibodies (Methiamzole; alpha lipoid acid)
- Most common in Asian females
- Idiopathic autoantibody
- Young, caucasian, F > M with other autoimmune disorders
- Insulin Receptor
- Genetic mutation – inherited
- Antibody to insulin receptor – acquired:
- Young, african american, F > M, other autoimmune features, PCOS features and LOW triglycerides.
- IGF-mediated – paraneoplastic
- Hepatocellular carcinoma
- Relative adrenal insufficiency
- Has a particular propensity for hypoglycemia
- Adrenal insufficiency
- Glucagon deficiency
- All of the above can occur with above.
- Warburg effect
- Increased consumption by highly aggressive tumors – usually lymphoma
- Liver disease
- Renal disease
- Rarely meet Whipple’s triad criteria
- Avoid in renal impairment
- Beta-blocker toxicity.
- Central lines are in the right atrium and so we are often measuring the central (not mixed) venous oxygen saturation. This correlates well, but not perfectly, with the mixed venous oxygen saturation.
Approach to SvO2
- The tissue ischemia that develops in a hypotensive patient prompts increased oxygen uptake and leads to a low mixed venous oxygen saturation.
- Therefore when the SvO2 is high (>70%) is a hypotensive patient, there is a concomitant impairment in oxygen extraction – this is a hallmark of sepsis where pathologic vasodilation and mitochondrial toxicity impair O2 extraction.
- Other causes of high SvO2 includes
- Arteriovenous shunts (no capillary bed to extract O2)
- Liver disease (portosystemic shunting)
- Mitochondrial toxicity
- Thiamine deficiency
- Cyanide poisoning
- Meds (Linezolid)
- Inherited mitochondrial disorders
- A low SvO2 occurs in all the other kinds of shock
- Low central venous pressure
- High central venous pressure
- High central venous pressure