As easy as … airway and breathing

Given that the new batch of house officers have just started, it seemed like a good time to update this blog. Today’s post is the first in a two part series about the ABCs. When called to the bedside of an unwell patient, the advice given is to “attend to the ABCs” first. Without further explanation of what the ABCs actually entail, this is only minimally helpful. Today we shall focus on the first two letters.

The best way to start is to make explicit that the lung really only has two functions. The first is to maintain an appropriate blood level of oxygen. Appropriate can be considered to be an oxygen saturation somewhere in the 90s. Now, an oxygen saturation of 92% may not be normal, but it is generally sufficient for the purposes of oxygen delivery to organs. The second is to get rid of CO2. More specifically, to maintain a CO2 of 40mmHg (around 5kpa).

These two processes proceed very differently. To get oxygen into blood one needs an open alveolus and a capillary that supplies it. The blood flow through that capillary must be appropriately matched to the amount of oxygen in the alveolus- if the blood flow is too much for the amount of oxygen in the alveolus, the blood in that capillary will be desaturated. This explains why you can have patients who are much more hypoxic than you might expect from looking at their chest xray. Collapse of alveoli occurs on a microscopic level and is not necessarily visible on chest Xray. Many patients are on vasodilatory medications (antianginal or antihypertensives) that impair their ability to match capillary blood flow with the amount of oxygen in the alveolus. It can also be easy to miss collapse of an entire lobe on xray unless you know what you are looking for. The relevance of this is that it is easy to go on a wild goose chase of other causes of hypoxia if you believe that the Xray must correlate with the patient’s clinical condition. Consider the following case.

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Avoiding harm: the early postoperative fever

One of the most important principles in medicine is to avoid doing harm to your patients. This is easier said than done because sometimes things that are iatrogenic are confused for natural evolutions of the disease process. That leads to writing the first post in a series entitled ‘avoiding harm’.

One good example is the early postoperative fever. I use this term to mean fever occurring in the initial 24-48 hour post operative period. As a house officer my friends and I spent many hours taking blood cultures on these patients, obtaining chest X-rays and chasing urine samples.

Eventually I realised what would happen is we would treat areas of atelectasis that were confused for pneumonia, colonised (but not infected) bladders and skin contaminants on blood culture. All of this represented unnecessary exposure to antibiotics, which have the potential to seriously harm patients.

Fortunately all of this can be avoided. There are 11 articles in the literature which I have taken the time to find for you. They uniformly tell us that if there is no sign of focal infection on clinical exam, the ‘septic screen’ can be safely forgone.

Blood cultures were the most useless. In four studies the pick up rate on blood cultures (excluding contaminant results) was zero. Two of these studies were designed specifically to look into the utility of blood cultures. All studies had large numbers of patients. One study found that of 38 blood cultures only 1 was positive and this was on post-operative day 16. Two further studies reported a 6-7% rate of positive blood cultures. The pick up rate of chest Xrays and urine cultures was about 10%.

Four studies reported that in those patients who were diagnosed with an infection, the majority of the time the source was identifiable based on physical exam and clinical picture, or that the clinical picture guided the need for further investigations.

Three studies actually attempted to quantify the cost. One calculated a cost of $8000 per change in clinical management, one worked out $2000 per infection diagnosed and one concluded that “rote” ordering of tests resulted in a total of $20000 (or $278 per patient) excess expenditure. All eleven studies concluded that “routine” ordering of investigations for early post-operative fever was unnecessary and costly.

  1. Sivakumar B, Vijaysegaran P, Ottley M, Crawford R, Coulter C. Blood cultures for evaluation of early postoperative fever after femoral neck fracture surgery.  J Orthop Surg (Hong Kong). 2012 Dec;20(3):336-40.
  2. Bindelglass DF, Pellegrino J. The role of blood cultures in the acute evaluation of postoperative fever in arthroplasty patients. J Arthroplasty. 2007 Aug;22(5):701-2.
  3. Lesperance R, Lehman R, Lesperance K, Cronk D, Martin M. Early postoperative fever and the “routine” fever work-up: results of a prospective study. J Surg Res. 2011 Nov;171(1):245-50. doi: 10.1016/j.jss.2010.03.009. Epub 2010 May 11.
  4. Fanning J, Neuhoff RA, Brewer JE, Castaneda T, Marcotte MP, Jacobson RL. Yield of postoperative fever evaluation. Prim Care Update Ob Gyns. 1998 Jul 1;5(4):146.
  5. Petretta R, McConkey M, Slobogean GP, Handel J, Broekhuyse HM. Incidence, risk factors, and diagnostic evaluation of postoperative fever in an orthopaedic trauma population. J Orthop Trauma. 2013 Oct;27(10):558-62.
  6. Ward DT, Hansen EN, Takemoto SK, Bozic KJ. Cost and effectiveness of postoperative fever diagnostic evaluation in total joint arthroplasty patients. J Arthroplasty. 2010 Sep;25(6 Suppl):43-8. doi: 10.1016/j.arth.2010.03.016. Epub 2010 May 10.
  7. de la Torre SH, Mandel L, Goff BA. Evaluation of postoperative fever: usefulness and cost-effectiveness of routine workup. Am J Obstet Gynecol. 2003 Jun;188(6):1642-7.
  8. Athanassious C, Samad A, Avery A, Cohen J, Chalnick D. Evaluation of fever in the immediate postoperative period in patients who underwent total joint arthroplasty. J Arthroplasty. 2011 Dec;26(8):1404-8. doi: 10.1016/j.arth.2011.02.019. Epub 2011 Apr 7
  9. Czaplicki AP, Borger JE, Politi JR, Chambers BT, Taylor BC. Evaluation of postoperative fever and leukocytosis in patients after total hip and knee arthroplasty. J Arthroplasty. 2011 Dec;26(8):1387-9. doi: 10.1016/j.arth.2010.12.024. Epub 2011 Feb 25.
  10. Verkkala K, Valtonen V, Järvinen A, Tolppanen EM. Fever, leucocytosis and C-reactive protein after open-heart surgery and their value in the diagnosis of postoperative infections. Thorac Cardiovasc Surg. 1987 Apr;35(2):78-82.
  11. Freischlag J, Busuttil RW. The value of postoperative fever evaluation. Surgery. 1983 Aug;94(2):358-63.

Hyponatremia Part 2: Managing it

The first step when confronted with a low sodium is to ask yourself if it is real. There are two interpretations of the word “real”. Firstly the machine at the lab may have spat out an incorrect result. This occurs if there is excess protein or lipid in the sample, because it affect the calculations made when the sample is diluted. This is not true of blood gas analysers- the blood gas sodium is accurate on a blood gas.

The other is to ask does this actually reflect a low serum osmolarity. We don’t care about hyponatremia so much because of the low sodium itself, but because we assume it reflects low serum osmolarity overall. It is this that actually causes all the troubles of cerebral oedema etc. Most of the time this is a correct assumption because serum osmolarity is

formula

Most of the time the other components don’t play a huge role. But if the glucose is sky high, or you have another osmotically active particle such as mannitol, water will be sucked out of the cells, diluting the sodium. The sodium in this case is “real” however is doesn’t really matter because the overall plasma osmolarity is raised due to the presence of mannitol or craploads of sugar.

An easy way to eliminate this possibility is to check a serum osmolarity.

At the end of the first section we discussed people who had excessive sodium losses. Now, even though these patients might be losing a lot of sodium from the GI tract or the respiratory tract the sodium concentration of these losses is still always LESS than plasma sodium concentration. The total amount of sodium being lost is high but the sodium concentration of lost fluid is still low. So how do these patients become hyponatremic?

Well firstly one of the responses of the kidney to hypovolemia is to activate vasopressin and hold onto free water. However patients with hypovolemia also tend to hold onto sodium – a urine sodium < 20mmol/L fits with hypovolemic hyponatremia. So this doesn’t fully explain it. Even when urinary sodium reabsorption is inhibited, as you might see if the cause of hypovolemia is diuretics, the urine sodium rarely gets above 100mmol/L. So the renal response to hypovolemia of holding onto free water does not fully explain why the sodium drops.

It’s because people continue to drink water, usually from the tap, and the thirstier they feel the more they drink.  In short water and sodium are both lost, the water is replaced, the sodium is not, and the renal response prevents the free water from being excreted. Voila, low sodium levels. However without an ongoing exogenous source of water, hyponatremia will not develop.

So hypovolemic hyponatremia presents with low urine sodium levels, unless the cause is diuretics, or some other form of renal loss, such as acute tubular necrosis where the tubules are damaged, cannot retain sodium and put out vast quantities of urine. One could of course examine the patient and determine that they are hypovolemic as the textbooks advise, but anyone who has worked in clinical medicine for more than 2 minutes will realise that when it comes to differentiating between hypovolemia and euvolemia, one might as well do a rain dance, summon the gods, and ask them what they think. People who are confident in their ability to clinically differentiate between the two are probably deluded.

So the treatment is to expand the plasma volume with a resuscitation fluid and remove the stimulus for vasopressin secretion. Free water will be able to be excreted and the sodium will rise. You should probably do this cautiously- dumping a lot of fluid into someone often removes the vasopressin stimulus quite rapidly and an alarming diuresis can result, one that raises the sodium by more than the 8mmol/24 hours that safety recommends.

It would actually make complete sense to volume expand someone intravenously while at the same time restricting their oral fluid intake. Given that salt water tastes disgusting we tend to drink mostly free water, so expanding someone with salty water while limiting their free water intake is perfectly logical. Maybe best avoided however as people will give you weird looks and if you’ve already induced a diuresis adding on a free water restriction might overcorrect the sodium.

The classic cause of euvolemic hyponatremia is SIADH. The same pathophysiology that we already discussed applies, except this time vasopressin release is stimulated in the absence of hypovolemia, so the kidneys will not be holding onto sodium, and the urine sodium will be > 40mmol/L. However as mentioned, renal losses of sodium from diuretics or ATN will give the same urine chemistry, and this is a common pitfall. SIADH is actually not that common in patients presenting from home. It is more common is postsurgical patients where vasopressin is released due to the surgical stimulus and in little kids who become sick.

Hypervolemia should be more obvious clinically. The pathophysiology here is once again the same except the stimulus for vasopressin release is the sympathetic response to a failing heart. Diuresis is the treatment of choice here. It probably works because frusemide induces a loss of “salty water” and “free water”, but more “free water” and the patient is prevented from taking excessive free water because we usually fluid restrict people who are overloaded. Reducing atrial stretch and the neuroendocrine response to this also probably plays a part.

In all of these conditions the urine osmolarity will be higher than serum because the kidney is reabsorbing water. If the urine osmolarity is low the patient is likely to have psychogenic polydipsia.

If your patient has acute neurological symptoms a bolus of hypertonic saline is in order, and you should ask for help on how to do this.

Lastly you may wonder why the chloride is low- given that chloride is the main anion that balances the cations in the plasma, it is inevitable that a low Na+ leads to a low Cl-.

Hopefully this gives some better understanding of why hyponatremia develops and how to manage it. The key is really understanding the difference between salty water and free water.

Hyponatremia Part 1: Salt versus free water

Hyponatremia is difficult to understand. So I’ve decided to devote two whole posts to unravelling this enigma. The first part deals with normal salt physiology and the often forgotten difference between salty fluids and free water, while part 2 will deal more with the management.

It is important to distinguish between salty water and free water. Salty water refers to your resuscitation fluids like normal saline, Hartmann’s and plasmalyte, which contain 140-150mmol/L of Na. Because they are isotonic with body fluids, these fluids will be confined to the EXTRACELLULAR space, which you might recall is about 15L in a 70kg male. Turns out having fluid that stays in the extracellular space is a good thing if your goal is to expand the blood volume.

In contrast free water is solute free fluid which is hypotonic. Therefore it will distribute itself among TOTAL BODY WATER, which again you might recall is about 40L in a 70kg male. Now, we don’t often give pure water intravenously, but we do give fluids like 5% or 10% dextrose. This essentially functions as free water because the glucose will be taken up by cells leaving the free water component. From the point of view of the blood compartment, this free water is a muddy pig- it slips its way out of your grasp and disappears into the vast expanse of total body water, which is why it is wholly useless for resuscitating someone. The commonly used fluid dex-saline (which is 4% dextrose plus 0.17% saline) contains some salt but one can kind of think of it as free water also.

Herein the questions arises of what kind of fluid do we lose everyday? Most people will remember that the daily requirement for fluid is about 2-3L per day. But what is the composition of this fluid? Does it matter?

confusion

Of course it does. A human’s daily requirement for Na is about 70mmol. Read that again. That’s not 70mmol/L. That’s 70mmol TOTAL. So you are losing far more water than you are sodium (relative to normal body concentrations). This is from sweat, respiratory losses, the GI tract and the kidneys. Even though the kidneys can produce highly concentrated urine, they still lose more water than they do sodium. Another factoid you might recall is that the normal urine sodium concentration is 20mmol/L. Even if you are being hammered with a diuretic and losing lots of sodium in the urine, the urine sodium might get up to 80-90mmol/L, but this still falls far short of normal plasma sodium concentrations.

Given the above information it reasons that the function of the 2L of maintenance fluid we chart patients who are nil by mouth should be to maintain plasma osmolarity (given that salt is the main determinant of this). Therefore one should prescribe a maintenance fluid that achieves this, which is the reason that dextrose saline is favoured. Going without maintenance fluid will steadily raise your plasma osmolarity/sodium.

The purpose of 2L of maintenance fluid is not really to maintain blood volume (assuming your patient is euvolemic to begin with). Of course it fulfils this purpose to a degree but the more important determinant of blood volume is the solute load. A sodium load activates vasopressin which allows us to reabsorb water in the kidneys. Water follows sodium in the kidneys and this “sodium attached water” stays in the extracellular space, allowing maintenance of blood volume. As mentioned however the daily sodium load required to achieve this is only 70mmol/day (pretty much what you get with two bags of dex-saline).

The last two paragraphs may be confusing, so let me recapitulate. To maintain blood volume your kidneys must reclaim a certain amount of “water attached to sodium” or “salty water”, and this reclamation is dependent on an adequate sodium load and adequate water intake. However most of the fluid lost by your kidneys is actually “sodium free water” which must be replaced orally or intravenously to maintain serum osmolarity. Of the 2-3L a day of “fluid” one loses (not just from the kidneys), most of it is in the form of “sodium free water”, while “salty water” is a smaller component.

So what happens if I give a euvolemic patient normal saline as maintenance? In order to cope with the solute load (one bag already has twice the daily sodium requirement) and maintain a normal serum sodium concentration the kidneys will activate vasopressin and hold onto more water. The amount of “salty water” will increase, while the amount of “sodium free water” the kidneys can excrete is reduced. The serum osmolarity will be maintained, but at the expense of an expanded extracellular fluid volume. This may not be so much of an issue in healthy patients but you can bet it will significantly increase tissue oedema in those with heart failure, or with inflamed leaky capillaries. People with good kidney function will be able to increase the sodium loss in their kidneys, but remember even when they are losing heaps of sodium in the urine they are still losing more water than they are sodium. The effect will be worse in those with impaired kidney function who are less able to increase urinary sodium losses.

Of course such a maintenance regime may be appropriate in those with ongoing sodium losses. Those with ongoing sodium losses will have trouble maintaining their extracellular fluid volume (and therefore their blood volume) so ongoing sodium replacement will be appropriate. These patients may have vomiting, diarrheoa, losses from stomas or fistulae or renal losses from diuretics or acute tubular necrosis. Which brings us to managing hyponatremia in Part 2…

The folly of chasing urine output with fluid in sepsis

Through medical school and house office years it is easy to develop many ‘reflex’ responses to certain conditions. Treating low urine output with fluid is one of these.

This makes sense in certain conditions. Hypovolemia leads to reduced renal perfusion. Correcting hypovolemia is therefore a good thing. Aggressive fluid resuscitation to restore renal perfusion makes sense in conditions where the patient is significantly fluid deplete, like enteritis or DKA, or where diuresis is helpful to prevent nephrotoxicity such as rhabdomyolysis or tumour lysis syndrome.

Unfortunately this has been extrapolated to every condition associated with AKI, resulting in massive fluid volumes being given to patients in the hope that the fluid will somehow drive the kidneys to work better. This is entirely devoid of physiological sense. This is most apparent in septic conditions. I particularly recall patients on the surgical ward with pancreatitis, who were given fluids for their oliguria and renal failure until they were swollen like the Michelin Man.

Chest Journal has published an article this month (1) addressing fluid management in acute kidney injury. This narrative is supported by a 2017 article of the same name. There are a few things to note.

Firstly, there is really no scientific evidence that macrovascular renal blood flow is routinely compromised in sepsis. Septic patients may be hypovolemic due to fluid shifts into the extracellular space but generally the problem is one of vasodilatation. The pathophysiology of acute kidney injury in sepsis is complex and involves tubular apoptosis and dysfunction at the cellular level.

river

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Why is hypoxia not part of the Wells Criteria?

Whether you have done medical or surgical runs you will have spent plenty of time trying to figure out whether a patient has a pulmonary embolism. Many clinicians will hang their hat on the presence or absence of hypoxia. You may then wonder why hypoxia is not actually part of the esteemed Wells criteria.

Well, it turns out the presence of hypoxia in PE is quite variable. In fact, not uncommonly patients with massive PE may have normal oxygen saturations, a phenomenon confirmed both by the literature (1) and my own observations. To understand why, we have to understand why hypoxia might occur in the first place.

It has actually taken a while for people to figure out why hypoxia occurs in PE, although it is still not 100% transparent. Many people assume that the problem is V (ventilation)/Q (perfusion) mismatching, where Q is decreased due to the obstruction. This is not quite correct. V > Q results in hypercarbia, but not hypoxia. The problem is that Q is redistributed to other lung units, without a matching rise in V. This results in regions of lung with low V/Q, away from the embolism (2,3). This seems to be the most likely cause of hypoxia.

This explains why massive pulmonary embolism may not cause hypoxia. Remember that massive pulmonary embolism is defined by the presence of RV strain and cardiogenic shock. If most of the pulmonary arterial tree is obstructed there is nowhere for the blood to be redistributed, minimizing the ability for areas of low V/Q to form. Additionally, if the patient has cardiogenic shock, low cardiac output reduces Q, reducing the inequality. Therefore, paradoxically, improving oxygen saturations may be a sign of worsening shock (4).

Hypoxia is therefore not correlated with the severity of pulmonary embolism. Patients with severe PE may not be hypoxic. If your patient appears shocked, or just looks terrible, you cannot use the absence of hypoxia to rule out PE.

On the other hand, small PEs may also not cause hypoxia, if they are too small for significant redistribution of pulmonary blood flow to occur.

All of this leads onto the next point, which is the utility of ABGs when you suspect PE. No doubt at some point you will have been asked to obtain an ABG in a patient where PE is suspected. The origins of this were some small, flawed studies suggesting that a normal A-a gradient on an ABG could rule out PE in combination with other features. This has been proven false in a more rigorous study (5) – a normal A-a gradient is equally likely in patients with or without PE initially suspected of having PE. This study concluded that ABGs had limited diagnostic value in the investigation of PE. Hopefully now you understand why.

Additionally most of these ABGs are requested on patients in whom it is clearly obvious from the end of the bed that there is an elevated A-a gradient. If you are on 5L of oxygen to maintain normal saturations and there is no clinical reason for hypoventilation, then you will have an elevated A-a gradient.

Till next time…

 

  1. Intensive Care Medicine. June 1977, Volume 3, Issue 2, pp 77–80| Cite as Massive pulmonary embolism without arterial hypoxaemia Pathophysiology in two cases. F. Jardin, J. Bardet, A. Sanchez, F. Blanchet, J. P. Bourdarias, A. Margairaz.
  2. Pulmonary Circulation. Gas Exchange and Pulmonary Hypertension following Acute Pulmonary Thromboembolism: Has the Emperor Got Some New Clothes Yet? John Y. C. Tsang, James C. Hogg First Published June 1, 2014 Review Article.
  3. Journal of Applied Physiology. Pulmonary embolization causes hypoxemia by redistributing regional blood flow without changing ventilation. William A. Altemeier, H. Thomas Robertson, Steve McKinney, and Robb W. Glenny. 01 DEC 1998https://doi.org/10.1152/jappl.1998.85.6.2337
  4. Hemodynamic Factors Influencing Arterial Hypoxemia in Massive Pulmonary Embolism with Circulatory Failure FRAN(OIS JARDIN, M.D., FRANCIS GURDJIAN, M.D., PIERRE DESFONDS, M.D., JEAN-LUC FOUILLADIEU, M.D., AND ANDRI MARGAIRAZ, M.D. Circulation 59, No. 5, 1979.
  5. Diagnostic Value of Arterial Blood Gas Measurement in Suspected Pulmonary Embolism. MARC A. RODGER , MARC CARRIER , GWYNNE N. JONES , PASTEUR RASULI , FRANÇOIS RAYMOND , HELENE DJUNAEDI , and PHILIP S. WELLS. https://doi.org/10.1164/ajrccm.162.6.2004204   PubMed: 1111212 Received: April 24, 2000

You’re taking the piss

Urinary tract infections are the scapegoat of the medical world. They make us lose our common sense, because once you find something that is easy to treat, you stop looking for anything else. This is termed satisfaction of search.

Let us look at two examples where a positive urine sample may lead the ward house officer astray, related to the domain of surgery.

Firstly, you have a patient who is POD4 after an anterior resection. You are called because they have become febrile. There is no obvious source on examination. You take cultures, and the mid stream urine comes back with a high number of white cells. You start the patient on cefuroxime for a presumed UTI. This is a frequent occurrence.

Unfortunately this decision neglects the basic rule of general surgery. This rule states that the main differentials in a febrile patient after abdominal surgery are as follows; anastomotic leak, anastomotic leak,  anastomotic leak and also anastomotic leak.

“But the urine is positive!”

Unfortunately pyuria is common in intraabdominal sepsis, presumably due to the infection rubbing up against the wall of the bladder and causing inflammation. The rate of sterile pyuria in appendicitis and diverticulitis for example can be anywhere from 25% to 70-80%, depending what literature you read (1,2).

This phenomenon is not even confined to intra-abdominal infection. 30% of patients presenting with pneumonia, sepsis, intra-abdominal infection, or enteritis have pyuria (3). Of these urine samples, only 30% were culture positive. Note that culture positivity does not imply a UTI- there will be a significant proportion of asymptomatic bacteriuria.

The second situation will be when you are not on general surgery, but convincing the surgical registrar to review your patient who has abdominal pain and a clinical presentation concerning for something surgical.

“But the urine is positive, why don’t you just treat the UTI?”

Take home message? Pyuria is common in patients with other serious sources of infection and you should remind yourself and others of this.

Till next time….

  1. Ther Adv Urol. 2015 Oct; 7(5): 295–298. Sterile pyuria: a forgotten entity. Sanchia Goonewardene and Raj Persad
  2. 09 Sterile Pyuria an Indication of Acute Appendicitis in Children. S. Lewis1, C. St. Laurent1, A. Ruiz-Elizalde1 1University Of Oklahoma College Of Medicine,Oklahoma City, OK, USA
  3. Sterile Pyuria in Patients Admitted to the Hospital With Infections Outside of the Urinary Tract. Jared B. Hooker, MS2, James W. Mold, MD, MPH, and Satish Kumar. JABFM March 2013:97-103

 

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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Bowel obstruction is a clinical diagnosis

You: “Hello Mr/Mrs. Surgical Reg, I’ve got a patient up here on the ward who’s started vomiting tonight and he hasn’t passed flatus for 24 hours and he’s got a tender tummy and I’m worried about a bowel obstruction”

Surgical Reg: “What does his abdo Xray show?”

You: “Its normal”

Surgical Reg: “Well why do you think he has a bowel obstruction then? The Xrays normal!”

Unfortunately when you create work for people, they can sometimes be less than helpful.

Now if you knew the sensitivity of an abdominal Xray, you could answer this question with ease.

This 2007 study (1) showed the sensitivity and specificity to both be about 82%. Second year radiology registrars had sensitivities as low as 59%, while senior radiologists reached up to 93%. Only 29 out of 90 patients had CT proven SBO. CT was the gold standard.

This study (2) used enteroclysis as the gold standard. This involves injecting a contrast material through a NJ tube and taking Xrays. This showed a sensitivity and specificity of 69% and 57%. If you are observant, you might have realised the implication of the numbers going down when a different gold standard is used- CT must not be so great either. Indeed, in this study the sensitivity and specificity of CT were only 64% and 79%.

Part of the explanation for these numbers is that Xray did better at identifying high grade obstructions (86% sensitivity) than low grade obstructions (56% sensitivity). The usefulness of the CT was in showing the cause of the obstruction rather than being far more sensitive.

In contrast (pun intended) this 1999 study (3) showed CT to have a sensitivity and specificity of 93% and 100%, while plain films were 77% sensitive and 50% specific. The gold standard was diagnosis from operative findings (25/30 patients) or by contrast study or clinical follow up, whatever that means, in the remainder.

Lastly this 1997 (4) review article is very informative and worth a read. It describes how the term ‘non-specific gas pattern’ means different things to different people! For example 65% of radiologists use the term to mean ‘probably normal’, 22% mean ‘can’t tell’ and the remainder mean ‘abnormal but not sure if ileus or mechanical obstruction’. What useful terminology!

They identify another analysis (page 1173, paragraph 2) where the sensitivity of plain films was only 66% when read by experienced radiologists; 21% of patients with ’normal’ findings had low grade obstruction.

So we can see that the accuracy of Xrays in the diagnosis of SBO varies a lot depending on the study, but to me seems generally underwhelming. At most the sensitivity in the hands of an experienced radiologist is 93% when compared to CT. It is important to remember however that the usefulness of the sensitivity/specificity depends on the pre-test probability- if your patient is vomiting and not farting and distended, the pre-test probability is high, therefore even with a high sensitivity there will be a large number of false negatives.

Clinical suspicion is important- radiography is a diagnostic aid, not the final arbiter. Always be guided by your clinical findings.

 

References:

  1. William M. Thompson, Ramsey K. Kilani, Benjamin B. Smith, John Thomas, Tracy A. Jaffe, David M. Delong and Erik K. Paulson. Accuracy of Abdominal Radiography in Acute Small-Bowel Obstruction: Does Reviewer Experience Matter? American Journal of Roentgenology. 2007;188: W233-W238. 10.2214/AJR.06.0817
  2. Reliability and role of plain film radiography and CT in the diagnosis of small-bowel obstruction. D D Maglinte, B L Reyes, B H Harmon, F M Kelvin, W W Turner, Jr, J E Hage, A C Ng, G T Chua and S N Gage. American Journal of Roentgenology. 1996;167: 1451-1455. 10.2214/ajr.167.6.8956576
  3. Comparative Evaluation of Plain Films, Ultrasound and CT in the Diagnosis of Intestinal Obstruction. Sudha Suri, S. Gupta, P. J. Sudhakar, N. K. Venkataramu, B. Sood & J. D. Wig. Acta Radiologica. Volume 40, 1999 – Issue 4. Pages 422-428
  4. The role of radiology in the diagnosis of small-bowel obstruction. D D Maglinte, E J Balthazar, F M Kelvin and A J Megibow. American Journal of Roentgenology. 1997;168: 1171-1180. 10.2214/ajr.168.5.9129407