Why it’s important to question authority, even in medicine

Last night I was watching one of those air crash disaster shows. For 60 minutes it followed the case of Comair flight 3272, which crashed in 1997 on its approach to the airport, killing all 29 aboard. While I get bored of the constant analogies drawn between medicine and the aviation industry, I found that this case imparted a powerful lesson.

For those of you who are regular readers (hopefully there are some!) you may have noticed a pattern in my blog posts- they often advocate challenging commonly held wisdom that may come from your seniors. It has not escaped my attention that this is one of those ‘easier said than done situations’. Comair flight 3272 will help me expound why I think this is important, and how to go about it.

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Why shock is not all about the blood pressure

shock

When calling the surgical or gastro registrar on the phone, one of the surefire questions you will be asked is ‘is the patient hemodynamically stable?’ This is no doubt an important question but unfortunately hemodynamic stability means different things to different people. There is generally a lack of willingness to look beyond a ‘normal’ vs ‘low’ blood pressure.

It should be made clear that hypotension is a sign of ‘decompensated’ shock. The idea that hypotension is a late sign of shock has been long recognized in the trauma literature where 18% of penetrating abdominal trauma can have over 750ml of blood in the abdomen despite normal vital signs (including 7% who had over 1500ml). In the majority of patients evidence of tissue hypoperfusion precedes the development of hypotension (1).

Why is this? Well, it is all about the concept that pressure does not equal flow. The body is quite adept at trying to maintain a normal blood pressure through various compensatory mechanism, chief amongst which is the sympathetic response. But this does not tell us whether perfusion at the tissue level is adequate- inadequacy of this is after all the definition of shock. This is especially true in young patients where the compensatory mechanisms are quite strong and blood pressure may be preserved till late in the piece, as illustrated by the graph at the top, of my creation (credit to MS paint).

This phenomenon is true in all situations- not just trauma- so it is relevant to the patients you will be seeing on ward calls. For example ‘normotensive shock’ is recognized in sepsis (2), cardiogenic shock (3), and just generally (4). What then are the signs of ‘normotensive shock’ you should look out for? Well, these are simply the signs of inadequate tissue perfusion- cool and clammy skin, oliguria, mental state changes and elevated lactate. Other signs which may accompany this that are not necessarily indicative of hypoperfusion but that do indicate a compensatory response are tachycardia and tachypnea.

It is also important to note two slightly related things. Firstly, a systolic blood pressure of 110 may be normal for a 20 year old but grossly hypotensive for a 70 year old with chronic hypertension. Secondly, it is sometimes difficult to tell whether a ‘soft’ blood pressure in a young person is just normal for them or whether they are actually hypotensive- a normal heart rate cannot be used to reassure you in this instance because not uncommonly shocked patients may have paradoxically increased parasympathetic tone (1) the exact mechanism for which is unclear. Older patients may also be on Beta Blockers.

The conclusion in all of this- next time you call the gastro reg with a patient who has vomited blood and is clammy with a lactate of 4 but has a normal blood pressure, the answer to the question ‘is the patient hemodynamically stable?’ is a ‘HELL NAH”.

Today’s post may sound basic but it is all about fundamentals- a fundamental which is often simply not done. Rather than spending 10 minutes documenting dual heart sounds, look and feel for the signs of shock!

Till next time.

 

 

  1. Identification and Resuscitation of the Trauma Patient in Shock Michael N. Cocchi, MDa , Edward Kimlin, MDa , Mark Walsh, MDb , Michael W. Donnino, MD. Emerg Med Clin N Am 25 (2007) 623–642
  2. Septic Shock. Advances in Diagnosis and Treatment. Christopher W. Seymour, MD, MSc and Matthew R. Rosengart, MD, MPH. JAMA. 2015 Aug 18; 314(7): 708–717.
  3. Menon V et al. Acute myocardial infarction complicated by systemic hypoperfusion without hypotension: Report of the SHOCK trial registry. Am J Med 2000 Apr 1 108 374380
  4. Approach to Hemodynamic Shock and Vasopressors. Stefan Herget-Rosenthal, Fuat Saner and Lakhmir S. Chawla. CJASN March 2008, 3 (2) 546-553; DOI:https://doi.org/10.2215/CJN.01820407

Tricky gut ischemia, the uselessness of lactate, and the importance of clinical suspicion

You are called to see Ms A, an 80 year old woman on the surgical ward, due to worsening abdominal pain and tachycardia. She was admitted 8 hours ago with the same abdominal pain and diarrhea and had a CT abdomen, which the radiology registrar has provisionally reported as showing non-specific pericolonic fat stranding. She has been treated as an infectious colitis. She has a history of ischemic heart disease, atrial fibrillation and claudication. Examination of her abdomen shows diffuse tenderness but no peritonism.

You call the surgical registrar to express your concern this lady might have ischemic gut. He informs you he is reassured by the CT findings, the lack of peritonism and the normal lactate, which you had decided to check because you have recently heard about the association between gut ischemia and elevated lactate. When you arrive at work the next morning you discover that overnight she had become septic, spiked her lactate to 8 and been taken for a laparotomy, where extensively necrotic bowel was found. She was palliated.

Ischemic gut is one of those diagnoses that is always tricky to make, as there is no lab test to help you and the examination findings can be non-specific, although “pain out of proportion to the exam” is what you might find in the textbooks.  Age confers an exponentially increasing risk, and past the age of 75 it becomes more likely than appendicitis or ruptured AAA (1). This is a fact which I certainly hadn’t appreciated and I suspect many people don’t, given the frequency with which we query the latter two on CT requests and the infrequency with which we query ischemic gut.

The first point to make abundantly clear is that peritonism is a late sign of extensive bowel necrosis so is not reassuring. The same applies to the finding of portal venous gas on an abdominal Xray, pictured below (2). The whole point is to diagnose the condition early enough that you can do something about it (either open or endovascular revacularisation). By the time these signs develop, the proverbial train has left the station.

portal venous gas

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Measuring Blood Pressure

Since hypotension is probably the most common “serious” ward call you will be asked to see, it is somewhat dispiriting that zero time is spent in medical education going over how the tools we use to measure this important parameter actually work.

If you’ve sat in on any tutorial on managing hypotension you will likely have been exposed to the old chestnut that if a patient’s radial pulse is palpable their systolic is at least 80, and if their femoral is palpable then it is 70-80, and if the carotid is palpable it is 60-70, or some other similar variation on these parameters.

How accurate is this seemingly simple bedside guide? Unfortunately not very! This (1) elegant study compared arterial line blood pressure measurement with assessment of pulses (done by blinded assessors). The graph below (reproduced without any permission) shows the expected blood pressures in green shading based on which pulses are palpable (groups 1-4), while the scatter points shows the actual systolic blood pressure recorded. As you can see, the degree of hypotension was severely underestimated by the above rules.

sbp

However, while the presence of a radial pulse is not reassuring, it would still appear that the absence of one is probably correlated with severe hypotension. Therefore if your BP cuff is not able to record the blood pressure, and you cannot feel radial pulses, it is not a machine fault! For some reason people stop trusting machines when they give extreme readings.

Speaking of which, it is worth understanding how automatic BP cuffs actually work. The machine is actually an oscillometer, which measures oscillations in the brachial artery that are transmitted through the air filled tubing. The mean arterial pressure (MAP) is determined when the amplitude of the oscillations is maximal. Above and below the MAP, the amplitude of oscillations will decline, and the systolic and diastolic are determined when the amplitude reaches a certain percentage of the maximal amplitude (see the figure below for an illustration). The reason this is important is that the cutoff for systolic/diastolic is determined based on a mathematical formula, so it is estimated in a way (2).

oscillomneter.png

 

Where this becomes relevant is thinking about how reliable your NIBP is in hypotension. This study (3) looked at correlation between NIBP and invasive arterial line measurement in 150 ICU patients, about half of whom had circulatory failure with hypotension or needing vasopressor drugs. They found that non-invasive measurement of MAP was pretty accurate, especially when the patient was hypotensive. However, non-invasive systolic and diastolic measurements were not accurate, with the systolic pressure often being overestimated.

What about manual blood pressure? The literature provides very divergent evidence, but it seems that in the population that we are interested in (the hypotensive) that automated cuffs overestimate the systolic blood pressure, sometimes to quite alarming degrees, at least if this study of trauma patients is to be believed (4). Manual blood pressure is better correlated to injury severity and markers of shock in this group.

The interesting corollary to this is that the often employed delay tactic by house officers when paged about hypotension, of asking the blood pressure to be repeated manually in the hope that it will give a more encouraging reading, is a waste of time. If the automatic cuff is sized properly, any hypotension should likely be believed.

The conclusion of the second part of this article is basically

  • Either learn to work with MAP rather than SBP, or…
  • If you can’t be stuffed doing the above or find it too difficult, then use a manual to assess the SBP; automatic cuffs are unreliable for this parameter and will overestimate it in the setting of hypotension.

Till next time…

 

  1. Charles D Deakin and J Lorraine Low. Accuracy of the advanced trauma life support guidelines for predicting systolic blood pressure using carotid, femoral, and radial pulses: observational study. BMJ. 2000 Sep 16; 321(7262): 673–674.
  2. https://lifeinthefastlane.com/ccc/non-invasive-blood-pressure
  3. Lakhal K, Macq C, Ehrmann S, Boulain T, Capdevila X. Noninvasive monitoring of blood pressure in the critically ill: reliability according to the cuff site (arm, thigh, or ankle). Crit Care Med. 2012 Apr;40(4):1207-13. doi: 10.1097/CCM.0b013e31823dae42.
  4. Are automated blood pressure measurements accurate in trauma patients? J Trauma. 2003 Nov;55(5):860-3. Davis JW1, Davis IC, Bennink LD, Bilello JF, Kaups KL, Parks SN.

 

The Hb in acute bleeding

bleeding

Imagine you are called to review a patient who has started vomiting blood an hour ago. You arrive to find them tachycardic with a heart rate of 110. Amongst all the other stuff you would do for this patient, you check an Hb. Its 130, unchanged from baseline. What does this tell you about the severity of the bleed?

The answer is nothing at all. Zilch. De nada.

The reason for this is explained brilliantly in the chapter on acute blood loss anemia in the book Clinical Haematology: Theory and Procedures (1) and supported by more recent articles (2).

When blood is lost from vessels, it is both plasma and red cells that are lost in equal numbers. Therefore acutely the haemoglobin concentration will not change. What is responsible for the haemoglobin dropping is shift of fluid from the extravascular space to the intravascular space in response to reduced intravascular volume, thus diluting haemoglobin.  It can take 48 hours for the full effect of this to be seen.

The earliest haematological findings that are seen are actually an increase in the platelet count which can take place in as little as an hour. Soon after a neutrophilia with left shift of white cells develops. The latter can take 2-4 days to resolve.

So in the above example, don’t be reassured by the fact that the Hb is normal, even though many times even your seniors will try and tell you “the patient can’t be bleeding significantly because there is no haemoglobin drop”.  In fact, the presence of a resting tachycardia, as in the above example, indicates fairly significant blood loss, potentially consistent with greater than 750ml if the classification of shock systems are to be believed.

The other corollary to this is that you don’t base the decision to transfuse blood on the Hb level, but rather on the patient’s clinical progress/your assessment. The full ins and outs of this are something that is difficult to discuss in a blog post. Additionally, the presence of thrombocytosis or neutrophilia/left shift can give you clues to the presence of bleeding when you are unsure, as they develop quite early.

References:

  1. Clinical Hematology: Theory and Procedures, Volume 936. Mary Louise Turgeon. Lippincott Williams & Wilkins, 1999. Pages 116-119.
  2. Clinical review: Hemorrhagic shock. Guillermo Gutierrez, David Reines and Marian E Wulf-Gutierrez. Critical Care2004(8):373

Supine masking of hypotension

tburg

Today’s post regards a common pitfall regarding the assessment of the hypotensive patient. Unfortunately, it will be based on anecdote rather than literature, but hopefully you won’t find the underlying assumptions too controversial.

Often you are called to the bedside of a patient with a hypotensive episode. You arrive to find them flattened on the bed, sometimes in the Trendelenburg position. You take stock of the situation and find the airway to be intact, the patient fully responsive, with warm peripheries and a good strong peripheral pulse. They are breathing comfortably. A blood pressure is taken and this is 110/70. The other vitals are normal as is the rest of the examination.

It is easy to conclude that the blood pressure has normalised and that this was therefore a self- resolving period of hypotension, most likely postural or vasovagal. What is important to remember is that, if you leave at this point, you have left the patient in a highly unnatural position. People don’t live their lives supine, nor indeed in Trendelenburg, and often their previous blood pressure recording taken in hospital will be with them sitting up. It is easy to gloss over this fact as you only arrive after the fact and therefore tend to only ever see the patient supine.

Before being reassured that the blood pressure is normal you must make sure it is normal in the sitting position. If they are sat up and now the blood pressure is 85/40, you clearly have an ongoing problem. Even the most posturally fragile old patients should maintain a normal blood pressure while sitting.

I have certainly ignored my own rule multiple times and it is extremely easy to do so because the human mind tends to only see what is there in front of you. Also, given the multitude of calls for abnormal vital signs, we latch onto any indication that the patient is actually OK and doesn’t need intervention. A few times when I ignored this rule I was later called for sustained hypotension (of course after they had been sat up) which turned out to be proper pathology.

The first of many lessons that you always need to take into account what we have done to the patient when making your assessment!

Asthma- avoiding common pitfalls

Asthma is quite an interesting condition to treat acutely, not only because it is gratifying when patients get better rapidly (which most of them do) but also because they are a group that can deteriorate quickly and hide their signs of deterioration well given their young age and relative health.

Given the nature of the disease it is not uncommon for patients to feel much better after being treated down in ED, then get worse again on the ward, perhaps as the frequency of their B agonist therapy is reduced. It is therefore imperative to avoid the common pitfalls when called to see these patients on the ward. The information below is directed at adult patients, but a lot of it will also apply to paediatrics too.

Asthmatics can die quickly

asthma phenotypes
Credit: Reference (1)

If you look at near fatal asthma cases two distinct phenotypes emerge as seen in the table above- the group that worsens over several days and whose pathology involves mainly mucus plugging, and the group who mainly develops bronchoconstriction with very rapid deterioration but faster responses to therapy. The latter are more commonly known as brittle asthmatics.

It is this group that are particularly relevant to ward calls as respiratory failure can develop in as little as 2 hours, and death is often sudden and unexpected (1). Such patients often show marked diurnal variation in peak flow, especially a large dip in the early morning, even when their previous peak flow was normal (1). Looking back at a patient’s previous discharge summaries and clinic letters should help you identify who might fit into the “sudden onset” phenotype.

In hospital death is not related to admission findings but is related to the phenotypes above

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