Tag Archives: SFVA

VA ICU Report: Post CABG Complications

This morning the inimitable Simon Ascher (not Nancy’s son), Vivek Murthy (Not the surgeon general), and Ashish Agrawal (anesthesiologist extraordinaire) presented an interesting case of a gentleman w/ stable CAD who had a 3v CABG and some post-operative complications. A great interdisciplinary case.

MI Schema (for funsies and pedantry)

Type 1- ACS (UA, NSTEMI, STEMI)
Type 2- Demand ischemia
Type 3- Sudden cardiac death 2/2 MI
Type 4- MI after PCI (type 4b specifically stent thrombosis post PCI)
Type 5- MI after CABG

So we talked about a type 5 MI, for those of you who will be code leaders here are some pearls to take with you for post-CABG and valve replacement surgery

Cardiogenic shock post CABG (Thanks to Dr. London for these pearls)

-Myocardial stunning (often will be on inotropes post-op: dobutamine, epi, norepi)
-Bradycardia (often related to myocardial dysfunction though in valve cases can be related to direct injury of conduction system), often pts require pacing after surgery
-Hypovolemia: in particular “on-pump” CABG leads to dramatic fluid shifts post operatively and these patients can be markedly hypovolemic
-Tamponade: interestingly, because of the way the pericardium is manipulated intra-op blood will not flow freely in the fashion we are used to but will pool in the lowest pressure area of the pericardial sac, namely around the right atrium, reducing preload, and just like any tamponade case–>fluids to increase preload is life saving! IF needed a stat TEE can be done by anesthesia to visualize the hematoma, ultimately the treatment is surgery

Another clue to tamponade is the lack of output from the chest tubes, if blood isn’t coming out of the tubes it’s filling up somewhere else, either pleura or pericardium.

Last pearl for code leaders: Often codes involving post-op CT surg patients can be challenging, it’s imperative to work with our surgical colleagues as they can solve the above technical problems, but our knowledge and help can be important in these cases as well. Most important to-do for you: find the surgeon and anesthesiologist and discuss the plan, and whether they think the ACLS algorithm is appropriate given the clinical picture.

VA Report Pearls: Microcytic Anemia!

Pearl 1: A good way to think (and teach) about microcytic anemia is to consider the ways in which microcytosis occurs. RBCs become microcytic due to a lack of hemoglobin, which can result from:

  • Lack of iron (iron deficiency, anemia of chronic inflammation)
  • Defects in heme synthesis (sideroblastic anemias)
  • Defects in the production of hemoglobin protein (thalassemias and hemoglobinopathies)

Pearl 2: Remember that in thalassemia (unlike iron deficiency and anemia of chronic inflammation), the RBC count may be normal or elevated, since the bone marrow is making large numbers of small cells. 

See the attached review article from the NEJM for more on microcytic anemia!

Microcytic Anemia_NEJM

Evernote Link

VA Report: A practical approach to thinking about heart failure

At report today, Goop gave us a true pearl about his simplified approach to determining the etiology of heart failure. He pointed out that there are 4 main causes of heart failure – after that, there is a long list of other causes that are much less common (and not worth committing to memory!).

He suggested that we remember the top 4 causes, and feel comfortable looking up the rest when they become relevant.
The top 4 causes of heart failure are:

  • CAD
  • HTN
  • Valvular disease
  • Toxins/EtOH

Remember those four, and if the presentation does not fit, then go on to consider alternative explanations!

Evernote Link

4.20.16 – Dermatomyositis-Associated Malignancy

Dermatomyositis-Associated Malignancy

  • Dermatomyositis (DM) and polymyositis (PM) are both associated with malignancy with the association being stronger for DM >> PM.
  • Incidence of cancer for patients with DM is increased 5- to 7-fold compared to the general population.
  • Cancer can be diagnosed before, simulataneously with, or after the diagnosis of DM and PM though (as Rabih mentioned) the peak incidence of a cancer diagnosis in DM and PM occurs simultaneously with/during the first five years after diagnosis.
  • Types of malignancies = adenocarcinoma of the cervix, lung, ovaries, pancreas, bladder, and stomach accounts for 70% of cases.
  • With a new diagnosis of DM, the following labs are routinely performed:
    • CBC, LFTs, U/A
    • FIT versus colonoscopy for colon cancer screening
    • CXR
    • For women: pap, mammo, transvaginal U/S and CA-125 levels for ovarian cancer screening
      • Of note, there is no consensus on frequency of ovarian screening. Pap smears should be performed annually for patients with immunosuppression.

VA Report: Infectious complications of intravesicular BCG instillation

Bacillus Calmette-Guerin (BCG) is a live attenuated strain of Mycobacterium bovis that is administered locally for treatment of superficial bladder cancer. It is usually well tolerated, but rarely, there can be infectious complications – both local and systemic.

The pathogenesis is not completely understood, but it is theorized that the organisms gain access to the lymphatics and blood via disrupted uroepithelium, with the potential to disseminate to multiple sites.

Severe adverse events due to instillation of BCG for bladder cancer are uncommon (less than 5%).

Local Disease:
1) A mild cystitis develops in the majority of patients after instillation of BCG.

Systemic Disease:
1) The most common severe systemic disease is a high fever (>39 degC), in ~3% of pts
2) Other systemic complications of BCG instillation include:
Sepsis syndrome
Granulomatous hepatitis
Pneumonitis (interstitial or military pattern)
Osteomyelitis
Arthritis

The diagnosis of a BCG-related reaction can be difficult to confirm, as the mycobacteria are not always seen on acid-fast smears or cultures.

Here is a great CPC from NEJM on the infectious complications of BCG.

BCG Complications_NEJM CPC_1998

 

VA Report: Carbamazepine, HLA-B*1502, and SJS/TEN!

Pearl:
1) There is a strong association between the presence of HLA-B1502 and carbamazepine-induced SJS/TEN in Han-Chinese, Thai, and Malaysian populations.  

2) The FDA has recommended screening patients of Asian ancestry for the HLA-B1502 allele before starting carbamazepine.

3) Overall, carbamazepine is the most common cause of SJS-TEN!

Tangamornsuksan et al. Relationship between the HLA-B*1502 allele and carbamazepine-induced Stevens-Johnson Syndrome and toxic epidermal necrolysis. JAMA Dermatology. 2013;149(9):1025-1032.

 

Also, take a look at this figure for a great DDx of short-lasting headaches!

Short lasting HAMatharu MS, Goadsby PJ. Trigeminal autonomic cephalgias. J Neurol Neurosurg Psychiatry. 2002;72(Suppl II):ii19-ii26.

Evernote Link!

 

VA Report: Low SAAG ascites in cirrhosis!

The Pearl:
In patients with cirrhosis and a low pretest probability for non-portal hypertension-related ascites, a low SAAG has a poor predictive value.

Often, when the SAAG is repeated in these patients, it will return to a level >1.1!

In other words, many patients with cirrhosis and a low SAAG do not actually have a second reason besides portal hypertension for their ascites.  In a 2009 study of patients with cirrhosis and a low SAAG, Khandwalla et al. found that only a minority of these patients had a second cause (most commonly peritonitis or peritoneal carcinomatosis).

As such, the recommendation is to evaluate the other usual peritoneal fluid studies (e.g. cell count/diff, protein, cytology). If there is no clear secondary cause, it is reasonable to repeat the paracentesis – the aforementioned study found that on repeat testing, the SAAG often returned to the expected level >1.1!

NEJM Journal Watch

Khandwalla et al. The utility of evaluating low serum albumin gradient ascites in patients with cirrhosis. Am J Gastroenterol. 2009;104:1401-1405.

Evernote Link