M.D Physcian emergency medical and critical Care

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Last month, I posted a survey to  find out the Glasgow Coma Scale (GCS) values trauma centers were using to trigger their highest level trauma activation. Nearly 150 people responded, providing a nice snapshot of practices worldwide. Today, I’ll summarize the responses and provide a bit of commentary about them.

There were a total of 147 respondents from around the world. I tried to eliminate duplicates from the same center using a self-reported postal code. However, this was an optional field, so there is the possibility that a few crept in. Readers from at least six countries outside the US also responded.

The question  was: “What is the highest GCS score that triggers a top-level trauma activation at your trauma center?”

Here is a chart that shows the results. The proper way to read it is “a trauma activation is called if GCS < xx” where xx is the score under the bar in the chart.

The whole point to calling a trauma activation is to have the full trauma team and infrastructure (labs, imaging, blood, etc.) in place to rapidly assess a patient with life-threatening injuries. In theory this should afford them the best probability of survival.

So what is the optimal GCS score to activate your trauma team? Unfortunately, this remains difficult to answer exactly. From the chart, you can see that the most common scores were 8, 9, and 13. Why such a spread?

The GCS 8 and 9 levels are a no-brainer (ha!). These patients are comatose or nearly so, and obviously need prompt attention such as airway control, head CT, and neurosurgical consultation. But what about the patients with GCS 13? They have lost two points, typically for eye-opening and verbal response. This may indeed indicate  a significant head injury. But all too often we see this same score in patients who are intoxicated. Do we really need (or want) to activate the full team for each and every intoxicated patient? Can we screen them out in some way?

The answer to both questions is yes. The most important tip is to know your patient population. There is an association between GCS and need for operative intervention that was oft-quoted in the ATLS course. However, I have not been able to find a definitive paper on this topic.

I recommend that you tap into your trauma registry and create a chart that shows presenting GCS vs early neuro-intervention (ICP monitor or craniectomy within 24 hours). Find the GCS score where you see a “significant” bump in the number needing a procedure, and use this as your trauma activation threshold. This report will automatically take into account the number of intoxicated patients you treat.

I would also recommend you do a separate report on age vs need for neuro-intervention with GCS<15. The older population tends to require craniectomy for TBI more often and at higher GCS levels than younger people. You may factor this into your single GCS criterion, or add a separate one at a different level for patients over 55, or 60, or whatever reflects your patient age mix.

Bottom line: Make sure your GCS trauma activation criteria adequately identify your patients who truly have a need for speed in their trauma evaluation. A GCS of 8 or 9 may be too low, and a score in the teens is probably more appropriate for most centers. Use your trauma registry to determine the best score for you so you can capture the patients who have critical needs while trying to keep overtriage under control.

IO lines are a godsend when we are faced with a patient who desperately needs access but has no veins. The tibia is generally easy to locate and the landmarks for insertion are straightforward. They are so easy to insert and use, we sometimes “set it and forget it”, in the words of infomercial guru Ron Popeil.

But complications are possible. The most common is an insertion “miss”, where the fluid then infuses into the knee joint or soft tissues of the leg. Problems can also arise when the tibia is fractured, leading to leakage into the soft tissues. Infection is extremely rare.

This photo shows the inferior vena cava of a patient with bilateral IO line insertions (black bubble at the top of the round IVC).

During transport, one line was inadvertently disconnected and probably entrained some air. There was no adverse clinical effect, but if the problem is not recognized and the line is not closed properly, there could be.

Bottom line: Treat an IO line as carefully as you would a regular IV. You can give anything through it that can be given via a regular IV: crystalloid, blood, drugs. And even air, so be careful!

I’ve spent the last week discussing the hypothetical case of a young patient with a stab to the abdomen. I worked through some of the thought processes regarding physical exam, imaging, and choices for management. Fortuitously, it would seem, The Journal of Trauma published an algorithm on this very topic from the Western Trauma Association (WTA).

The WTA Algorithm Committee reviewed existing data to start the process of developing this algorithm. As could be expected, very little high quality data was available. So the final algorithm is a synthesis of existing lesser quality studies, expert opinion from the committee members, and commentary from the membership.

Here are some of the highlights:

Unstable patients go straight to the operating room (A)

Patients who cannot be examined (unconscious, head injured, intoxicated) should be evaluated for peritoneal penetration with local wound exploration, ultrasound, CT, or laparoscopy. If positive or equivocal, proceed to exploration. (B)

Patients who can be examined should be managed by location of the stab. Flank injuries are lower risk and should be scanned. Anterior stabs can be evaluated using observation, local would exploration, or CT scan,

Positive results generally proceed to laparotomy. The algorithm states that laparaoscopy “may be performed in select stable patients by a highly skilled surgeon experienced in minimally invasive surgical techniques.”

As with any algorithm or practice guideline, nothing is etched in stone. These tools are good for about 90% of the clinical situations you will encounter. If you end up off the beaten path, you will need to use your best judgment to provide best treatment for your patient. Just remember to document your rationale, because you may very well have to justify it to your peers.

Click the diagram below to see a full size version.

Reference: Evaluation and management of abdominal stab wounds: A Western Trauma Association critical decisions algorithm. J Trauma 85(5):1007-1015, 2018.

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Early tracheostomy is generally accepted to be a good thing in critically injured patients. A number of papers have shown that it decreases ventilator days and hence ICU and hospital days,  and also reduces pneumonia rates, sedation requirements, and saves quite a bit of money.

However, there has been one problematic group in whom critical care surgeons are often forbidden to do an early trach: patients with a recent anterior cervical fusion. These patients typically have unstable cervical fractures, with or without a concomitant spinal cord injury. The spine surgeons argue that doing a trach “too soon” leads to a higher infectious complication rate due to the proximity of the trach to their anterior surgical wound.

But is this really true? The trauma/critical care program at Thomas Jefferson University in Philadelphia looked at their experience. They are a federally sponsored spinal cord injury center, and have a vast experience compared to most trauma centers. They reviewed their experience over a 16 year period. Typically, they performed all of their tracheostomies within 10 days, so they arbitrarily defined “early” as within 4 days, and “late” as > 5 days after the cervical procedure.

Here are the factoids:

A total of 98 patients with tracheostomy after anterior fusion were included in the study, some of whom also underwent a concomitant posterior fusion

39 cases were “early”, within 4 days of the anterior fusion procedure, and 59 were “late”

Average time to fusion in the early group was 2 days, and 10 days in the late group

There were no wound infections in the early group

There were 5 wound infections in the late group, and 4 of them involved the posterior fusionsite(!)

The only infection of the anterior fusion site occurred in a late patient who suffered an esophageal perforation from the fusion hardware

Bottom line: Although the numbers are still small after 15 years of data, it’s probably the best we will ever get! It is clear that an anterior fusion wound is safe in these procedures. I am at a loss as to why the posterior fusion wounds tend to get infected, though. But the next time your spine surgeons balk about doing an early trach in one of their anterior fusion, show them this paper!

Systemic air embolism (SAE) is an uncommonly encountered but potentially catastrophic complication that trauma professionals will probably see only once or twice in their career. In a couple of very old papers (30-35 years!), it was said to occur in 4 to 14% of patients with severe lung trauma. The pathognomonic finding is complete cardiovascular collapse shortly after intubation and positive pressure ventilation of a patient with significant chest trauma.

SAE can occur after major blunt or penetrating injury. Normally, pressure in the pulmonary arterial and venous branches of the lungs is higher than that of air in the bronchi. If lung parenchyma is torn by gunshot, stab, or blunt pulmonary laceration, then blood can leak into the smaller airways. Unless a major vessel is torn, the volume lost is not of much consequence. A small amount of hemoptysis may be present.

But if positive pressure is applied to the airways, air may be forced into those vascular structures. If the injury involves a pulmonary vein, the gas bubbles enter the left heart and and then the systemic circulation. Only a cc or two of air in the cerebral circulation or coronary arteries can cause a rapidly fatal condition.

How can a trauma professional suspect that a patient may be susceptible to SAE? Look for evidence of hemoptysis in patients with penetrating chest injury or severe blunt chest trauma. Unfortunately, this occurs in only a few patients and its absence is not helpful.

Always suspect SAE if your patient suffers circulatory collapse or arrest shortly after intubation and positive pressure ventilation. This is especially true in patients who were very stable up until that point. Ultrasound may be used to detect air bubbles in the left heart. Transesophageal echo is even better, but not readily available in the ED.

What can be done if your patient (nearly) arrests after intubation and you suspect SAE? The recommended treatment is single lung ventilation and thoracotomy on the injured side. The injured side is obvious in patients with unilateral penetrating injury, but much more difficult to determine in blunt trauma where either lung may be involved. A quick chest x-ray could be obtained, but may not localize the injured lung.

If the left lung is involved, push the endotracheal tube into the right mainstem bronchus to eliminate the abnormal pressure gradient in the injured lung. If the right lung in injured, a dual lumen endotracheal tube should be inserted for single-lung ventilation. Unfortunately, this requires fiberoptic tools and is not available in the field or most emergency departments.

If single-lung ventilation can be accomplished, this may buy some time to try to resuscitate your patient. A thoracotomy of the injured side can also be carried out to occlude the hilum of the lung in an attempt to stop any further embolism. Initial clamping should be carried out by hand, as using a crushing clamp commits the patient to an emergency pneumonectomy (if they survive beyond this point).

Overall survival is dismal. Old data suggests that more than 80% of blunt trauma victims with SAE die, as well as half of patients with penetrating injury. These numbers are even lower once the patient arrests. The key to survival is avoiding unnecessary intubation in patients with potential SAE, and moving to single-lung ventilation quickly in those who have developed it.

Function

Similar in structure to a large lymph node

Acts primarily as a blood filter. 

Removes old red blood cells and holds a reserve of blood, which can be valuable in case of hemorrhagic shock

recycles iron 

as a part of the mononuclear phagocyte system, it metabolizes haemoglobin removed from senescent red blood cells (erythrocytes). 

 synthesizes antibodies in its white pulp and removes antibody-coated bacteria and antibody-coated blood cells by way of blood and lymph node circulation. 

Structure

The spleen contains two main regions of tissue called white pulp and red pulp.

Red pulp: Contains venous sinuses (cavities filled with blood), and splenic cords (connective tissues containing red blood cells and white blood cells).

White pulp: Mostly consists of immune cells (T cells and B cells).

Pathology

Enlarged Spleen (Splenomegaly): caused by eg viral mononucleosis (“mono”), liver disease, blood cancers (lymphoma and leukemia), etc

Ruptured spleen: can cause life-threatening internal bleeding 

Sickle cell disease:  inherited anaemia, abnormal red blood cells block the flow of blood through vessels and can lead to organ damage, including damage to the spleen. 

Thrombocytopenia (low platelet count): enlarged spleen sometimes stores excessive numbers of the body’s platelets. 

Accessory spleen: About 10% of people have a small extra spleen. This causes no problems and is considered normal.

ALP: 

Present in liver, bone, intestine, kidney, neutrophils and placenta. 

80% originates from bone. 

If GGT up, ALP from liver. 

If GGT normal, ALP from bones. 

ALP rises with obstruction to the biliary tract. 

ALT: 

Most present in the liver, but also found in other tissues. 

Very high levels suggest, viral hepatitis, diabetes, congestive heart failure, liver damage, bile duct problems, infectious mononucleosis or myopathy.

AST: 

Present in liver, heart, skeletal muscle, kidneys, pancreas, lungs, leukocytes and erythrocytes. 

Increased levels may indicate haemolytic anaemia, rhabdomyolysis, increased leucocyte count etc

Distinction in source can be made via CK and Troponin. 

AST<ALT = hepatic injury

AST>ALT = hepatocyte necrosis - poor prognosis (AST is found in the mitochondria, not spilled out until severe destruction) - CONSIDER MUSCLE SOURCE

AST:ALT Ratio: 

Greater than 2 = Hepatitis.

Less than 2= cholestatic disorder.

GGT: 

Found in both hepatocytes and biliary epithelial cells. 

Sensitive for hepatobiliary disease. 

5 times increase = good marker of alcohol abuse.

GST (Gluthathione S-transferase):

 Isoenzymes of GST are involved in the detoxification and conjugation of several electrophilic compounds with glutathione. 

Found to be a very good marker of acute hepatocellular damage with a half life of 90min. Not widely used.

CK: 

Found in heart, brain, skeletal muscle and other tissue. 

Released when muscle damage. 

Causes range from exercise injury to hormonal disorders.

LDH: 

Found in muscles, liver, heart, pancreas, kidneys, brain and blood cells. 

Used to used to diagnose and monitor heart attacks. 

Five types of isoenzymes can help determine location of damage. 

LDH-1 - heart, red cells, kidney, germ cells. 

LDH-2 - heart, red blood cells, kidney (lesser amounts than LDH-1).

LDH-3 - lungs and other tissues. 

LDH-4 - white blood cells, lymph nodes; muscle, liver (smaller amounts than LDH-5).

LDH-5 - liver, muscle.

Troponin: 

Highly specific marker for myocardial infarction or muscle cell death. 

Also used to diagnose other conditions which relate to cardiac muscle injury.

Lipase: 

Found in blood, gastric juices, pancreatic secretions, intestinal juices and adipose tissues.

Hydrolyses triglycerides  

Acute pancreatitis, pancreatic neoplasia, pancreatic abscesses, and pancreatic duct obstruction can result in high levels of lipase and usually are 2 to 3 times the upper limit of normal.

Amylase: 

Is made by the pancreas and by the glands in and around the mouth/throat. 

Catalyses hydrolysis of starch 

High amylase may indicate the presence of a condition affecting the pancreas. 

In acute pancreatitis the levels are 4-6 times normal and remains high until treated. 

Chronic pancreatitis, levels will be high but will decrease until problem is solved.

Acid phosphatase: 

A quick peek into the presentation and neurosurgical management of acute subdural haematoma (a type of bleed on the brain), with GoPro footage and medical illustration breaking down a craniotomy decompression.

Nice and visual for those curious about the pathology, presentation, and management of this life threatening complication of a head injury. 

Yes, more on predictions. We all know that chest trauma is one of the bigger causes of morbidity and mortality in trauma patients. A number of methods have been developed to predict which patients might deteriorate after sustaining chest injury, and where to place them in the hospital on admission. Elderly patients are at particular risk, and determining who to look after more closely, and/or in the intensive care unit, can be very helpful.

The authors of this abstract from West Virginia University took a slightly different approach. Let’s say we have already placed a patient in a ward bed after admission for rib fractures. How can we monitor them and preemptively increase interventions or move to the ICU before they crash and burn?

The WVU group developed a rib fracture guideline nearly 10 years ago, and retrospectively reviewed their experience with 1106 patients over a 6 year period. They measured serial forced vital capacity readings in these patients, and arbitrarily used thresholds of <1, 1-1.5, and >1.5 to predict deterioration.

To boost your memory, look at the following chart. The vital capacity is the maximum amount of volume that can be voluntarily exhaled.

Here are the factoids:

Only patients with initial FVC > 1 were enrolled in the study

They were then separated into two groups: those whose FVC remained greater than 1 (83%), and those in whom it decreased below 1 (17%)

Patients in the low FVC group had significantly more complications like pneumonia, intubation, or unplanned transfer to ICU (15% vs 3%) and a longer length of stay

However, the low FVC group also had a higher chest AIS score, higher ISS, were 10 years older, and were twice as likely to have COPD

Bottom line: Seems like a promising study, right? Check out an easy to measure, objective test and step up your level of care if it dips below a certain critical value? But not so fast. The two study groups look like they are very different. No significance testing was shown for these differences, but they certainly look like they should be different. Couldn’t their deterioration have been predicted based on their age and degree of chest injury?

Here are some questions for the authors to consider before their presentation:

Please provide the details of your rib fracture pathway

Your FVC threshold does not have any units assigned. I am assuming that it is in liters. Please clarify.

Why did you describe three cohorts initially, then settle on the lowest (FVC < 1) as your final threshold? Was there a method to this? Why not 1.5? Or 0.75?

Did you do any further analysis to try to determine if the differences between the groups were responsible for the differences in complication rates?

Big picture question: So why couldn’t you just use a specific age/ISS/comorbidity threshold and predict failure at the time of admission, and forget about measuring several FVC values?

Reference: EAST 2018 Podium paper #9.

Christian Symbolism in Renaissance Flowers

In Europe during the Renaissance (about A.D. 1400–1600), Christians looked to nature for spiritual enlightenment and to guide their contemplation of the divine. In illuminated manuscripts made during the period, intricately painted landscapes or flora and fauna were often represented as aids to prayer.

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For decades, plasma (with vitamin K) was the mainstay for reversing warfarin. Over the past several years, prothrombin complex concentrates (PCC) have made inroads in the management of this problem because of its sheer speed of action.

There are two problems with plasma. First, most hospitals still have only fresh frozen plasma (FFP), and it takes 20-30 minutes to thaw. This adds some up-front time to administration. Then, it takes time to infuse the 250cc or so of volume in each unit. This may be 1 or 2 hours, depending on policy and patient tolerance of a bolus of colloid.

If it always just took one unit of plasma to correct the INR to a desirable range (typically 1.5-1.6), then the whole PCC conversation might be moot. You could potentially have the INR corrected in 30-60 minutes depending on your patient’s cardiovascular system.

But how many does it really take? A group at Eastern Virginia Medical School in Norfolk, VA looked at this problem and tried to come up with a mathematical formula. They examined a year of warfarin reversal data at their hospital. Patients with severe clotting disturbances (advanced cirrhosis, DIC) and those who received additional products (PCC or activated Factor VII) were excluded.

Using data from nearly 1,000 patients, the following formula was derived and validated:

∆ INR = (0.57 ∙ preINR) – 0.72

So a patient with an INR of 3.0 would be expected to show a decrease of 0.99 to about 2.0 after one unit. This formula can be used iteratively to figure out how many units will drop the INR to the goal range.

I don’t know about you, but I hate doing math in the middle of a trauma resuscitation. I need something quick and dirty. A physician from NYU Langone in NYC commented on the article, and derived a nice little table to simplify the process. He calculated the number of plasma units based on some common INR ranges, assuming that the goal was to get it down under 1.5. Here is the table:

Bottom line: This is a nice little piece of information to tuck into your pocket or phone. For patients inside the usual therapeutic values, it will take 2-3 units of plasma to reverse. For your average older human with average comorbidities, expect this to take 4-6 hours, not counting ordering, thawing, and delivery. If my definitions of “life-threatening bleeding” are met (see below), your patient may have significant adverse events during this time frame. So think very seriously about using PCC instead.

Related posts:

What’s the INR of FFP?

Life-threatening bleeding in the anticoagulated patient

Reference: Fresh Frozen Plasma Dosing for Warfarin Reversal: A Practical Formula. Mayo Clin Proc 88(3):244-250, 2013.