emergency medicine iceland

Nov 16, 2014

Male with abdominal pain and a flabbergast passenger

This case of a gentleman with lower abdominal pain is interesting not only clinically, but more so through the prism of basic cognitive science and how it applies to clinical judgement. We take a closer look at how we are prone to making mistakes due to heuristics and cognitive biases. Also included are some gems on the obvious usefulness of ultrasound at the bedside and a gentle reminder about interpreting an elevated D-dimer result. Sit back, grab a 'kókómjólk' and enjoy the case.

Abdominal pain

51 y/o B. F. with prior history of appendectomy in childhood presented to the ED with abdominal pain after referral from his GP.

The pain was localized to the left iliac fossa and had been intermittently increasing during the last week. It was coupled with increasing abdominal distension. No acute changes noted on the day of his visit. No fever or chills. Denies nausea and was not sick in the last week. He experienced runny stool earlier in the week and was constipated for 2 days but had a normal bowel movement yesterday without any blood or mucus. No bowel changes in the last months and no urinary tract symptoms. Noticed reduced appetite, did not eat since yesterday. B. F. also believed he had been losing weight over the last couple of weeks.

On physical examination the patient looked tired but in no acute distress. Vitals were all normal. Moderately distended abdomen, diffuse tympany. Bowel sounds present but faint and distant. Diffuse pain on pressure but no tenderness or guarding.

Cue in bedside ultrasound

Bedside ultrasound of the abdomen was performed. Visualizing was complicated by substantial amounts of air in the GI tract. Liver appeared normal without any suspicious growths on gross examination. Noted significant dilation of small bowel mostly in left flank with fluid contents and hyperperistalsis (like a "nest of worms").

At this point there was a strong consideration of ileus or at least subileus and since patient had distended abdomen a feeding tube was placed but which drained only 230 ml of GI fluids. Patient received 5 mg of Morphine.

What are the diagnostic criteria for small bowel obstruction on ultrasound examination?
  • Dilated bowel loops > 25 mm
  • Increased intraluminal fluid
  • Characteristic alternating peristalsis
  • Keyboard sign (visible plicae circularis)
  • Tanga sign (circumscribed free fluid)

The sensitivity and specificity of detecting a dilated bowel with bedside US after a merely 10-minute training session is 91 and 84 %, respectively. Compared to the 50-80 % diagnostic accuracy of a plain CXR, otherwise most commonly used at the ED for establishing the diagnosis. For further info see Jang et al. - Bedside ultrasonography for detection of small bowel obstruction in the emergency department.

A short but excellent introductory video tutorial on performing the examination can be found here and is presented by the legendary Chris Fox, emergency physician with a fellowship in ultrasound and book author - he is by far one of the best ultrasound teachers and all his lectures can be found online for free - FOAM at it's best! The small bowel exam starts at 13:30.

An informative and more academic post on SBO and the whole ultrasound vs other modalities, even a CT/MRI scan, can be found on Academic Life in Emergency Medicine, an incredibly useful site in general.

Putting the pieces together

Blood panel came back normal (WBC 5.000) aside from an elevation of CRP at 60 mg/L. Liver enzymes normal and urine dipstick test clean.

Because of suspected ileus/subileus patient was sent for an abdominal CT scan to look for underlying cause (remember, ultrasound is excellent for finding ileus but bad for finding the cause).

Radiologist's answer for the CT image was that there was no ileus, no free gas and no free fluid in abdomen. The clinical scenario was not on par with the radiologist's answer so the images were reviewed and discussed with the on-call surgeon. We agreed there were indeed partially dilated small bowel loops, "sentinel loops" and the surgeon was even concerned about some mesenterial veins being prominent, possibly suggest mesenteric venous thrombosis (MVT).

What are sentinel loops?
A sentinel loop is a focal area of adynamic ileus close to an intra-abdominal inflammatory process. The sentinel loop sign may aid in localizing the source of inflammation. For example, a sentinel loop in the upper abdomen may indicate pancreatitis, while one in the right lower quadrant may be due to appendicitis.
For more go to Radiopedia or RadiologyMasterClass.

CT abdomen; frontal, coronal and sagittal views

Incidentally the prostate is calcified.

Are prostatic calcifications always pathologic?
No. Prostatic calcification is most often an incidental, asymptomatic finding but it can cause symptoms such as dysuria, infection, haemautira, obstruction or pelvic/perineal pain. Occasionally calcifications can be passed via the urethra.
    Prostatic calcification may be either primary (idiopathic) or secondary to:
  • diabetes mellitus
  • infections - e.g. tuberculosis or bacterial prostatitis
  • benign prostatic hypertrophy - calcification occurs in 10%
  • prostate cancer
  • radiation therapy
  • iatrogenic - urethral stents or surgery
Radiopedia has more information on prostatic calcification.

A d-dimer was ordered which came back 2.890 ng/mL. A venous blood gas was also taken but came back within expected limits.

What are the possible pathological and non-pathological causes of D-dimer elevation
    Pathological possibilities are manyfold and can make life harder for us when we order it beyond its intended use:
  • Acute coronary syndromes
  • Acute upper gastrointestinal haemorrhage
  • Aortic dissection
  • Arterial or venous thromboembolism
  • Atrial fibrillation
  • Consumptive coagulopathy – DIC, VICC
  • Infection
  • Malignancy
  • Pre-eclampsia
  • Sickle cell disease
  • Stroke
  • Superficial thrombophlebitis
  • Trauma
  • On the not-too-pathological spectrum are the following standard conditions:
  • Age
  • Cigarette smoking
  • Functional impairment
  • Post-operatively
  • Pregnancy
  • Race

A D-dimer should be ordered when we have a low pre-test probability for venous thromboembolism (VTE). The latter can be assessed with any of the scores available, usually the Wells criteria for DVT, which can be found on MDCalc.

Gotcha ...

As everybody's eyes were focused on the dilated bowels an important find was missed until the images were reviewed for the second time… a large fluid-filled urinary bladder measuring about 15x12x7 cm - even the radiologist made no mention of it!

B. F. was diagnosed with urinary retention and catheterised in the ED with 1.500ml of clear urine passing in a few hours.

It is interesting to note that B. F. passed urine about 2 hours before the CT study was performed and still had about 1000ml of fluid visible on the CT scan. His HPI also did not include any urinary tract symptoms but upon further inquiry he describes hematospermia but had not seen a doctor for this.

B. F. was admitted to general surgery for observation but as symptoms relieved the suspicion of MVT was aborted. Urology was consulted and patient diagnosed with overflow incontinence. Patient was sent home with a urinary catheter for 10 days and Tamsulosin 0.4 mg x 1.

At outpatient follow-up no cause was found for his retention - the prostate was described as normal on palpation and ultrasound and cystoscopy showed no pathology. Patient continued on Tamsulosin and had no further urinary events but noticed memory problems and was referred for further cognitive evaluation.

What clinical entity could explain this?
Non-pressure hydrocephalus - although unlikely since gait and memory problems normally present before incontinence.
What causes overflow incontinence?
Transient urinary incontinence is often seen in both elderly and hospitalized patients. The mnemonic DIAPPERS is a good way to remember most of the reversible causes of incontinence, as follows:
  • Delirium or acute confusion
  • Infection (symptomatic UTI)
  • Atrophic vaginitis or urethritis
  • Pharmaceutical agents
  • Psychological disorders (depression, behavioral disturbances)
  • Excess urine output (due to excess fluid intake, alcohol, caffeine, diuretics, peripheral edema, CHF, hyperglycemia or hypercalcemia)
  • Restricted mobility (limits ability to reach a bathroom in time)
  • Stool impaction

To pee or not to pee

Urinary incontinence is defined as the involuntary loss of urine that represents a hygienic or social problem to the individual. Urinary incontinence can be thought of as a symptom as reported by the patient, as a sign that is demonstrable on examination, and as a disorder. Urinary incontinence should not be thought of as a disease, because no specific etiology exists. The etiologies of urinary incontinence outlined above are diverse and incompletely understood.

Patients with urinary incontinence should undergo a basic evaluation including a history, physical exam and a quick urinalysis.

Here you can take a look at a nice drawing comparing different types of incontinence.

It’s important to note the dynamics of urine loss with overflow incontinence since the bladder isn’t just filled to the brim and then it just empties at a certain point.

On the contrary, the bladder constantly remains full but just leaks small amounts of urine over time. Patients might not even notice any abnormalities, as was the case with B. F. The basic workup is aimed at identifying possible reversible causes. If no reversible cause is identified, then the incontinence is considered chronic. The next step is to determine the type of incontinence (urge, stress, overflow, mixed, or functional) and the urgency with which it should be treated. With slowly developing or chronic obstructions, patients typically are older, with multiple comorbid conditions, and they present with overflow incontinence and report little to no pain. But all that being taken into account, this is usually not a problem for the ED and should be handled by the patient’s GP.

To err is human a.k.a. discussion

Now, the reader that made it all the way through might come to ask the question: “Why’d they chase the ileus diagnosis after doing an ultrasound, when they could’ve seen the bladder?”

This is a very valid question that opens up a further discussion of cognitive errors in clinical judgement. While doing bedside US the examiner might have gotten caught up in a possible diagnosis of ileus, focusing most of his attention on this eventuality. Once they noted a possible distended loop of bowel, they unknowingly paid less attention to the rest of the systems that might have been involved. This in turn led everyone to temporarily miss the overexpanded bladder that would have been clearly visible on US as well. This is called anchoring.

Anchoring occurs when we sink our teeth into a possible diagnosis and pursue it, while discarding other possibilities. It is a type of thinking much akin to the “horses and zebras” analogy.

It is the tendency to fixate on specific features of a presentation too early in the diagnostic process and to base the likelihood of a particular event on information available at the outset. This may often be an effective strategy. However, this initial impression exerts an overly powerful effect in some people and they fail to adjust it sufficiently in the light of later information. Anchoring can be particularly devastating when combined with confirmation bias.

Anchoring may lead to a premature closure of thinking. Patients may be labeled with an incorrect diagnosis very early on in their presentation. Diagnoses, once attached, are difficult to remove and may seal the patient’s fate. (Croskerry, 2002)

Heuristics? Metacognition? Reflection ... Argh, where’s my Ritalin? Just tell me how I can fix it!

Luckily some smart people have identified strategies to battle heuristics and cognitive biases.

First and foremost, as with all types of bias, we need to be aware at all times that we are prone to biased decision-making. This is called metacognition and it has been proven effective in the past.

Checklists. Checklists reduce cognitive load and can improve patient outcomes and safety. A properly structured and intelligently designed patient interview form that is thoroughly implemented in the work environment can help us avoid missing an important step. A very cool and accessible book on the subject by dr. Atul Gawande is The Checklist Manifesto.

Morbidity and mortality conferences are helpful in highlighting cases where cognitive error was the source of raised morbidity.

Clinical decision support (CDS) systems are emerging as a novel adjuvant to the classic approach to the clinical decision process. Modern solutions are integrated into the electronic health record (EHR) and can provide weighted suggestions to clinicians, based on multiparametric inputs. (Dinevski, 2011) One of the core objectives of the Meaningful Use project in the United States, that aims to incentivize EHR adoption is implementation of at least one CDS system.

Recent additions to the body of knowledge on this subject however emphasize the importance of a wider change of culture that must take place in order to not only reduce errors but to also become aware of them in a healthy manner that does not promote defensive medicine.

Four take home messages

1. D-dimer can tell you some things, but you wanna know which. In this case a follow-up measurement might be warranted to establish what the cause of the elevated D-dimer was, since ileus secondary to thrombosis was ruled out. Or was it ... (a CT venography was never done!)

2. Ultrasound is cool for diagnosing ileus. High specificity and sensitivity compared to plain film. Can be performed at the bedside in the emergency setting. Fast, cheap, no radiation. Need we say more?

3. We tend to make cognitive errors. Let’s not forget it. And with a bit of practice and vigilance we can avoid the most common pitfalls. We outlined some of the strategies above.

4. Overflow incontinence presents as otherwise asymptomatic lower abdominal pain. This is attributed to the fact that there is no de facto retention since patients pass urine “normally”. The patient will present with discomfort in the abdomen. The thorough and systematic ultrasound examination is key to establishing the proper diagnosis in such cases. Plus it seems wise to keep urinary retention somewhere on the roster of differentials for lower abdominal pain with both genders.

4. Overflow incontinence presents as otherwise asymptomatic lower abdominal pain. This is attributed to the fact that there is no de facto retention since patients pass urine “normally”. The patient will present with discomfort in the abdomen. The thorough and systematic ultrasound examination is key to establishing the proper diagnosis in such cases. Plus it seems wise to keep urinary retention somewhere on the roster of differentials for lower abdominal pain with both genders.

Further suggested reading


Ultrasound for SBO

Overflow incontinence

Clinical cognitive biases

Author: Jan Hansel, a 6th year med student from Slovenia, passionate about medical education, emergency medicine and music. A young FOAMer in training. [Editor's note: Jan visited our ED in August 2014 and not only practiced emergency medicine like a boss but also tried swimming in the cold Atlantic!]

Oct 1, 2014

Elderly patient with persistent hypoxia

We present an unusual case of hypoxemia that was difficult to diagnose. The clinical scenario contained several small clues which when added up could perhaps, in retrospect at least, have led to timely diagnosis if they had been identified earlier. As this is a condition often discrete yet important for the physician to recognize we have presented the case for others to learn from. It contains interesting learning points on how to approach the hypoxic patient. We have used the opportunity to review basic lung physiology relevant to the clinician.

A 75 year old female, smoker, presented to the emergency department in an ambulance after being found on the floor of her apartment. She was fully conscious but had left-side hemiparesis and dysarthria. She was dyspneic and complained about bilateral pain low in the chest, radiating to the back.

Previous history was of hypertension and “some kind of arrhythmia” and she was currently taking antihypertensive tablets, ASA and zopiclone. There was no history of lung disease.

Examination and labs

    General: Patient is awake,> Vitals on arrival:
    • BP 162/102, pulse 112/min
    • temp 37°C
    • RR 28/min, sat 84% with 6L O2 on a simple face-mask
  • Cardiac auscultation: normal
  • Pulmonary auscultation: prolonged expiration, bronchial sounds with fine crackles at the base.
  • Chest: A fresh bruise at approximately 6-7th rib on the left side, laterally to midclavicular line.
  • Neurological examination: dysarthria, flaccid hemiparesis of left side.
  • Labs:
    • WBC 8.6, CRP 29
    • Hemoglobin 170, platelets 115
    • Na 142 K 3.6 creatinine 73
    • D-dimer 8.47 (<0.25), CK 2.933
  • ECG: atrial fibrillation 108/min, otherwise normal
  • CT head: Old infarcts at basal ganglia bilaterally, old infarct in left temporal lobe. No fresh infarcts, no intracranial bleeding.

tPA was judged as not appropriate as time from onset of stroke was far too long. Admission to neurology was prepared but patient was stuck in ED as there were no beds available in hospital.

It was noted that she was persistently hypoxic and not responding to O2 despite general maneuvers (increased FiO2, sitting patient up).

Why is the patient be better oxygenated by sitting up?
V/Q and shunting physiology is complicated but it is quite clear that body position affects both ventilation and perfusion (eg. use of prone position for patients with ARDS in ICU). All in all, supine position tends to decrease patient's own breathing and collapse alveoli in posterior (dependent) part of the lung - this leads to increased 'physiological (right to left) shunting' which is otherwise discrete and nonsignificant in the healthy subject. Patient sitting up or with head elevated (20-30') will do more efficient breathing (ventilation) and open more alveoli and decrease V/Q mismatch.
[Phys. Ther. 1985] Effect of Body Position on Pulmonary Function

An ABG was drawn (with 10L of O2):

  • pH = 7.46
  • pO2 = 52mmHg (80-100)
  • pCO2 = 31mmHg (34-46)
  • HCO3 = 24 (22-26)
  • (calculated) SaO2 = 87%
How do you interpret the ABG?
Uncompensated, mild respiratory alkalosis and hypoxia. Patient is hyperventilating to compensate for hypoxic state. Notice that pCO2 is not elevated, an important clue in the underlying condition.
Does the patient need to be intubated?
This patient does not have an immediate need of endotracheal intubation but certainly has a risk of decompensating fast due to exhaustion from hyperventilating, further decreasing SaO2 and starting a downward spiral of rising pCO2 and acidosis. We should keep in mind that having a SaO2 of 86%, this patient is at the rim of the steep slope of the oxygen–haemoglobin dissociation curve and there is no room for further desaturation.

Hypoxia management - ABC first!

Endotracheal ntubation is not risk free and there are still other options to help this patient. Emergency physicians are trained to always have a plan B and C, being mentally prepared for intubation is wise in this scenario and the patient should absolutely be placed in the critical care bay where the airway wagon is near.

  • A - Airway: patient is awake and protects her airway, excluding need of nasopharyngeal (Guedel) airway
  • B - Breathing: patient breathes spontaneously and does not need BVM assisted ventilation. FiO2 is 100% but flow can be increased so we change from simple mask to 15L O2 on reservoir mask which theoretically can supply lungs with approximately 80% oxygen.
  • C - Circulation: is not a problem here, she has minor tachycardia but not so that it reduces carriage of O2 to tissues.

This is a good time to review possible routes of oxygenation, although FiO2 from wall is 100% it can be difficult to provide the patient with air 100% saturated with O2 molecules.Oxygen therapy devices

Plan B - high flow O2 in nasal cannula!

Using the nasopharyngeal route for oxygenation has until recently been thought to provide only limited O2 to the lungs but airway guru Richard Levitan has proven otherwise and his work has led to game changers in approaching the desaturated patient. These two articles introduced the main publication in layman language; [EpMonthly] The neglected orifice [EpMonthly] No desat!

In our case we’d throw on 15L of 100% FiO2 with a nasal cannula and ensure patient is sitting upright - this simple maneuver would most likely be enough to prevent an unnecessary RSI. BIPAP is not recommended if patient is tired or drowsy but a CPAP trial could easily be done.

The articles mentioned above have been widely accepted by front-line emergency physicians as breakthrough publications for airway management and considered a must-read for every physician practising airway management especially RSI. The authors, Richard Levitan and Scott Weingart, are both highly respected teachers of airway and high-intensive care management and one of todays most wanted speakers in emergency medicine conferences. Luckily they are also advocators of FOAM and thus provide most of their material on the world wide web, free of charge!

Hypoxia workup

We now had time to focus on the cause of hypoxia. The patient had no fever thus pneumonia was considered unlikely. With the bruised left chest wall, pneumothorax was considered and bedside ultrasound done. The ultrasound found absence of lung sliding (not normal!) on left side so a chest x-ray was ordered to evaluate for suspected pneumothorax. Noticeably, there were no signs of pleural fluid and absence of B-lines, ruling out hemothorax and pulmonary edema.

What is the DDX for lack of lung sliding on ultrasound
  • pneumothorax
  • pleural effusion
  • massive consolidation/atelactasis
  • pulmonary contusion
  • advanced COPD
  • pleural adhesion/pleurodesis
  • severe fibrosis
  • if intubated
    • mainstem intubation
    • poor ventilation
    [Sonosite] Lung sliding explained

Bedside CXR showed no signs of pneumothorax but elevated left diaphragm and mediastinal shift to left side, indicating decreased left lung volume.

Formal radiologist review: “Decreased volume of left lung with shift of mediastinum and trachea to the left side. No evident infiltrates but suspected smaller peribronchial consolidations behind cardiac contour. No pulmonary stasis. “

Pneumonia could not be excluded even with lack of fever (remember elderly patients commonly have inappropriate vital signs) but ARDS was ruled out.

The meaning of mediastinal shift was not clear at this moment and the grossly elevated D-dimer value could not be explained so the next logical step was to have order a CT angiography of the lungs. Avid readers should by now be able to make a definite diagnosis as enough clues have stacked up!

What is the DDX for mediastinal shift?
  • 1. Pulled (loss of lung volume)
    • atelectasis
    • fibrosis
    • agenesis
    • surgical resection
    • pleural fibrosis
  • 2. Pushed (space occupying lesions)
    • pleural effusion
    • pneumothorax
    • large mass lesions
  • 3. Mediastinal masses and thyroid tumors
  • 4. Kypho-scoliosis

Radiologist's answer: "No sign of pulmonary embolism. Small consolidations posterobasally left side. No pathological lymph nodes. No pneumothorax."


IV antibiotics were initiated and we decided to consult the pulmonologist who then asked the radiologist to review the CT which on more thorough examination revealed a bronchial mucous plug (marked by red arrow at 0:28 in video). The patient went for bronchoscopy where the plug was drawn out and SaO2 rose.

Image of total bronchial cast (not from our patientFinal diagnosis: obstruction atelectasis secondary to mucous plug. Not surprising for a patient - a smoker - who has been lying immobilised for a longer time with pain in thorax, restricting air movement and dehydration contributing to the mucus buildup. Not unlikely she also has an undiagnosed, underlying COPD.

Finally - why was the D-dimer increased in this patient?
D-dimer is probably the single most incorrectly used lab test in the ED, commonly leading to unnecessary CTs. Remember, d-dimer was designed to RULE-OUT thrombosis in low-risk settings - the way we're using it today is no how it was supposed to be!
A study made 2007 demonstrated that immobility can elevate D-dimer titers by 50-60%. Other conditions and habits of the patient are also known to elevate D-dimer titres. Of the non-pathologic reasons include cigarette smoking and old age and pathological conditions including atrial fibrillation, stroke and infection. [LITFL] Dealing with d-dimer debacles


Pulmonary atelectasis is one of the most commonly encountered abnormalities in chest radiology and leads to a deflated lung segment or even whole lung collapse causing hypoxia. There are several different types of atelectasis, depending on the cause, as exlained below.

The video above shows how recruitment (=PEEP + ventilation) re-expands a deflated lung and helps us understand the importance of atelectasis. Lung collapse is atelectasis of the whole lung.

Atelectasis is primarily obstructive or non-obstructive, seperated mainly by their pathophysiology. Common causes of obstruction are foreign bodies, tumors and mucus plugs and the size of atelectasis mostly depends on where the obstruction is located (main-, lobal- or segmental bronchi). Obstructive atelectasis (the more common type) is also called resorptive atelectasis, refering to gas absorption distal to the obstruction. In a few hours this leads to retraction of the affected lung and ventilation-perfusion (V/Q) mismatch and shunting as circulating blood is not oxygenated. Secondary infection may occur. If the area is large there will be significant volume loss of the affected lung and secondary hyperinflation of the healthy lung leading to the distinct x-ray features of elevated diaphragm and mediastinal shift towards affected area.

Chronic atelectasis will eventually lead to fibrosis and widening of the bronchi, better known as bronchiectasis.

Non-obstructive atelectasis is caused by loss of contact between parietal- and visceral pleura and shares the same final outcome or total lung collapse. There are different types of non-obstructive atelectasis as well. Relaxation/passive atelectasis is caused by pneumothorax or pleural effusion, compression atelectasis caused by any-space occupying lesion within the chest and adhesive atelectasis by any disruption in surfactant, classically ARDS.

Atelectasis has many faces and the key to understanding its presentation, diagnosis and treatment is to know basic lung anatomy and the pathophysiologic mechanism. A detailed description of these can be found in the following excellent articles from eMedicine;AtelectasisPulmonary Atelectasis (pediatrics)

Atelectasis is a common concern in the ICU and post-operative ward. Decreased respiratory movements (eg. pain, diaphragma irritation), dehydration, O2 therapy and prolonged bed rest all contribute to atelectasis. The main methods to "recruit" alveoli are active adjustment of ventilator PEEP settings and the work of respiratory therapists encouraging patients to sit up and breathe properly with PEEP valves.

Symptoms and signs

They symptoms of atelectasis are subtle and non-specific; hacking, dry cough and sometimes mild fever. As atelectasis grows larger symptoms of hypoxia will dominate - cyanosis, dyspnea, tachycardia etc. On physical examination, dimishing breathing sounds may be the only clue.


Plain chest X-ray (PA) is usually enough to diagnose the presence of an atelectasis but does neither define the type nor the exact cause.

  • Direct signs:
    • displacement of interlobar fissueres (most reliable)
    • crowding of broncho-vascular markings
    • increased lung opacity (non specific)
  • Indirect signs:
    • hilar displacement
    • mediastinal shift
    • diaphragmatic elevation
    • Compensatory hyperinflation (if chronic)

In case of obstruction atelectasis air bronchograms are typically not present unlike the non obstructive types. The exact CXR signs to look for differ depending on which segment is involved. The signs are somewhat complicated, however, this short illustrated video gives an excellent explanation

A bedside chest X-ray (AP), as in our case has lower accuracy and will only reveal gross atelectasis and volume reduction of affected side. If there is a concurrent pleural effusion or large mass it can be difficult to define the cause of the atelectasis on CXR alone and CT is needed. CT scan will show the exact size, shape and location of the atelectasis. It can help in differentiating the obstructive type from the non-obstructive type, and serves as a guide for subsequent bronchoscopy. Although the obstructing lesion can be seen it may be difficult to define the exact cause, e.g. whether it is due to a tumor or a mucous plug. Such distinction will often require bronchoscopy and sampling of bronchial material by suction, endobronchial biopsy or transbronchial biopsy.[Radiopedia] Lung atelectasis

Systematic approach to hypoxia

The patient´s data included the following important clues in the systematic approach to hypoxia:

  • pCO2 was not increased and hypoxia therefore not caused by hypoventilation
  • A-a gradient was very high or 622mmHg (expected 21.5) excluding the cause to be low inspired O2 (see http://www.mdcalc.com/a-a-o2-gradient)
  • pO2 was not correctable by giving O2, suggesting shunt rather than V/Q mismatch and shunt is commonly caused by atelectasis, oedema, pneumonia or vascular shunt
Now wait a minute - what is the difference then between shunt and vascular shunt? Why doesn't pO2 increase with O2 when there's a shunt? It's time for a pulmonologist to explain some basic physiology! TIP: use Youtube's play faster feature for 1-2x playback speed (lower right corner)

Recommended reading on hypoxia: [The Medical Media Review] Hypoxia: Critical but Often Poorly Understood Concepts [Sashidhar Reddy] Hypoxia

Further reading

Life in the Fast Lane is one of the giants in the emergency medicine blogosphere and contains vast amounts of free teaching material for emergency physicians. It is one of our favorite websites. The LITFL guys have summarised all kinds of vital information for both new and experienced EPs;

Pulmonologist's comment

Great case with many aspects and learning opportunities! In brief, if I had seen the patient I would have been immediately worried about the severe hypoxemia with respiratory alkalosis, commonly seen in pulmonary embolism. Therefore a lung CT angiogram would probably have been my first radiology test (I certainly hope so, but these things are so much easier in retrospect), after seeing the blood gas result. No CXR needed and I agree, definitely NO D-dimer! But the CT is difficult to read.
The case reminds us how easy it is to miss the unexpected on imaging studies, and that we should remember to thank our good colleagues in that field on a daily basis.
To view another aspect, this is a smoker with a mediastinal shift on CXR. This combination should make us think about lung cancer with endobronchial involvement. This was appropriately ruled out by bronchoscopy. Mucus plugs are common, especially in chronically ventilated patients, in those with asthma and in those with hypoventilation in general. Conservative treatment with mucolytics and respiratory therapy is often sufficient, however bronchoscopic suction with the help of saline may be required to remove plugs. In severe cases, mostly encountered in the ICU, different types of bronchoscopic instruments may be needed to pull out large, dry, and amazingly hard plugs, such as the one depicted above. Large or small, it is important to follow up on the removal of plugs with mucolytics, bronchodilators and physical therapy for several days to prevent the common problem of recurrence. /Ólafur Baldursson


So it turns out that the patient had a mucus plug leading to a large atelectasis resulting in hypoxia. The underlying mechanism is shunting where a large obstruction hinders blood flow from pulmonary arteries and redirects it to other areas already well oxygenated. Thus no increase in SaO2 is seen despite high flow FiO2 on a rebreather mask. As described, normal pCO2 is also typical for this type of hypoxia as ventilation itself is mostly unaffected.

  • A chest X ray can be used to diagnose atelectasis but CT and/or bronchoscopy may be required to find the cause
  • A-a gradient, pCO2 and pO2 response to oxygen are important to find the underlying cause of hypoxia
  • Elevated D-dimer is specific for thrombosis but there are many other causes that need to be considered as well
Authors: Bergþóra Þorgeirsdóttir / David Thorisson

Sep 12, 2014

Young female with retrosternal pain and fever

Following is a case of a disease not so commonly encountered but worth knowing because of a concerning presentation - chest pain.

A female presents to the emergency department with a two day history of epigastrial pain. The pain is located right under the xiphoid process, and described as a sharp pain radiating through her chest and to the back. The pain is constant and worsens while lying on her back, on deep inhalation and when she eats or drinks. Lying on her left side alleviates the pain somewhat.

Her previous medical history includes Darier's disease (time to freshen up on your dermatology) and gastritis. Medications include Hydroxyzine (Atarax), oral contraceptive pill and isotretinoin (Accutane).

On examination there are no major clues as to her condition. Normal examination of lung­ and heart. Abdomen is non­distended, soft without guarding but diffuse tenderness mostly in the upper region. Bedside ultrasound shows no pericardial effusion, contraction is seen as normal and no signs of hypo- or akinesia. Gallbladder is not distended and no calculi are found. ECG is evaluated as normal with sinus rhythm, minimal inferolateral ST depressions and T ­inversions - concluded as nonspecific in the current clinical scenario. In the tachycardic patient with dyspnea pulmonary embolism could have been suspected.

Blood tests reveal slightly elevated CRP at 54 but other tests normal, Troponin T and d-dimer included. Chest x-ray is normal.

The morning after she develops fever 39°C. A trial of Gaviscon and Xylocain is unsuccessful. Augmentin 1,2g IV is administered empirically. On day three a gastroscopy is performed revealing multiple small, white, indented lesions in the esophagus. Candida infection is suspected and samples taken for PAD. CLO test is negative. She is suspected to have candida infection and admitted for treatment. The fever spikes occasionally up to 39.0°C but spontaneously resolves.

What do you think is causing retrosternal pain and fever in this young female?

Results come back from PAD and virology, surprisingly revealing an active infection with Herpes Simplex 1 (PCR positive). Other common causes of infectious esophagitis are candida and cytomegalovirus (CMV) and their presentation is similiar, requiring endoscopy for definite diagnosis.

A rare presentation for the above condition has been described where patient presented with intractable hiccups.

How are persistent hiccups defined and what are other important ddx to consider?

Hiccups for >48h are true 'persistent hiccups'. Many etiologies have been described but scaring ED physicians the most is the patient with ACS presenting as hiccups, it's been documented with several cases - enough for the lawyers to recognize it and the media to write about it. [Huffington Post 2012] Hiccups Were Patient's Only Heart Attack Symptom [Am J Emerg Med 2012] Hiccups as the only symptom of non-ST-segment elevation myocardial infarction

There are many treatment options and surely you should try rectal massage before pushing in that chlorpromazine!

Further reading

eMedicine has an extensive and excellent review as always [eMedicine] Esophagitis Amal Mattu as ever brilliant in his weekly ECG episodes, this time reviewing ECG findings in pulmonary embolism, do not start seeing patients in the ED until you have seen this! [Amal Mattu] ECG findings in pulmonary embolism

Authors: JMÆ/DBT

Jan 26, 2014

A shocking blood gas!

A healthy young man comes to the ED after having been chased by the police. They say he ran for his life at least 1km after which they found him lying down, presumably unconscious. With all systems intact and stable vitals he's presumed to be faking (pseudocoma).

A quick glance in the ED reveals nothing new to refuse this theory - the patient has closed eyes and is totally resistant to pain stimulation but has all reflexes intact (eg. gag, cornea-) and with eyes forced open he's looking straight forwards (to contrast with eg. roving eye movements if true coma). ECG comes in normal.

The police officers are informed that patient can return to police station as soon as blood results have been seen. And here they come...

With a hefty metabolic acidosis and lactate of 12,9 there's a minute of silence and doctors start thinking if there's a red herring in the room...

Could the patient be intoxicated after all?

Alcohols maybe?

He doesn't smell - but do all alcohols smell?

That's an anion gap of 18 - is it all explained by lactate?

With a presumed intoxicated patient fluids are ordered and patient is prepared for admission. Just that 45mins later the policemen come to let know that the patient is now awake and feeling well and ready to leave the ED with the officers. So a new blood gas (venous of course, who's sticking arteries these days anyways!) is drawn and voila;

All results normal... So the lactate acidosis turns out to be caused by strenuous physical exercise. Now howzaaat!

Learning points
  • Lactate can be very high after exercise! I remember a study where alpine ski-ers had 6-7 after coming down a slope and I've heard experienced clinicians state it may temporarily reach 20 after seizure). But you can even get disturbing pH levels from it!
  • Ethylene-glycol and methanol are odorless!

And my question to the audience: can I somehow calculate presumed anion gap from lactate levels, so that I can exclude other agents?

Acute dyspnea and bedside ultrasound

Elderly gentleman seeks the emergency department because of sudden dyspnea. He has no previous diagnosis of relevance such as COPD or heart failure. EMS notices crepitations on lung auscultation and treats patient with diuretics and CPAP with some relief. In the ED patient is still dyspneic and using accessory muscles for breathing but no clear crepitations are to be heard on auscultation and patient is not obviously obstructive. Stable vital signs, systolic blood pressure of 160mmHg.
Bedside chest x-ray is ordered but image result is not expected for a while. The ultrasound machine is turned on and the cardiac probe put on patient's thorax, revealing...

1. Heart, subxiphoid view

# Left > right ventricle => right strain and pulmonary embolism very unlikekly
# No pericardial effusion anteriorly, 2-3mm black line seen and assumed to be physiologically normal fluid
# Visually, decreased contractibility of left ventricle

2. Right pleura

Pleural effusion and several B-lines are clearly seen as the base of the lung reaches down, indicating right sided pulmonary edema

3. Left pleura

Great amounts of pleural effusion. No clots seen and thus no suspicion of blood. Multiple B-lines indicating left sided lung edema.

4. Right lung, apex

'Lung sliding' exludes pneumothorax. Multiple B-lines => edema reaches apex, suggesting massive pulmonary edema.

5. Left lung, apex

Same as right side; thus patient has massive, bilateral pulmonary edema.

The investigation was done in about 2 minutes.

The X-ray image arrives 45mins later

It shows enlarged heart with widened pulmonary veins and interstitial fluid bilaterally. Bilateral pleural effusion, more on left side. ProBNP arrives at 2500 with minimal Troponin elevation. Patient is treated as acute left sided heart failure and treated with CPAP and nitro infusion (SCAPE).

Previously, ultrasound has been said to be impossible to use for evaluating lungs, after all "air is ultrasound's greatest enemy". Experimenting with this has shown that indirect signs can be seen such as A- and B- lines and as air is replaced with consolidations and edema, ultrasound will immediately pick this up. For pneumothorax and pleural effusion, pulmonary edema and consolidations (pneumonia or ARDS), ultrasound is becoming a first choice for quick bedside evaluation. Increasing amount of data is supporting this and in some emergency departments, bedside chest x-ray has been replaced by ultrasound as only CT has better sensitivity for most conditions of relevance in the ED.

Acad Emerg Med. 2005 Sep;12(9):844-9
“The sensitivity for chest radiography was 75.5% (95% CI = 61.7% to 86.2%) and the specificity was 100% (95% CI = 97.1% to 100%). The sensitivity for US was 98.1% (95% CI = 89.9% to 99.9%) and the specificity was 99.2% (95% CI = 95.6% to 99.9%)”

Pleural effusion, pulmonary edema, consolidation:
Anesthesiology. 2004 Jan;100(1):9-15
“Auscultation had a diagnostic accuracy of 61% for pleural effusion, 36% for alveolar consolidation, and 55% for alveolar-interstitial syndrome. Bedside chest radiography had a diagnostic accuracy of 47% for pleural effusion, 75% for alveolar consolidation, and 72% for alveolar-interstitial syndrome. Lung ultrasonography had a diagnostic accuracy of 93% for pleural effusion, 97% for alveolar consolidation, and 95% for alveolar-interstitial syndrome. “

Let's summarize the data above:
AuscultationChest X-rayUltrasound
Pleural effusion61%47%93%
Pulmonary edema55%72%95%

Pulmonary embolism
The story of ultrasound becomes only better and better. Here, ultrasound is compared with CT for diagnosis of pulmonary embolism - the condition every physician fears to miss.
Chest. 2001 Dec;120(6):1977-83:
“The sensitivity of TS [transthoracic sonography] for detecting PEs was 80% (sensitivity of CT scanning, 82%), and the specificity of TS for detecting pulmonary lesions was 92%”

Volume status and heart - ultrasound for evaluation for shock
With ultrasound, a rough estimate of cardiac function and volume status (~vena cava status) can be done in instant. Together with above mentioned evaluation of thorax, ultrasound can in only 2-3 minutes give the physician a reliable diagnosis of acute dyspnea or shock. Add to this testing for free abdominal fluid, evaluating aorta and DVT diagnosis of lower extremities and then we have a full RUSH protocol (also known as FATE):
 RUSH: Rapid ultrasound for Shock and Hypotension

Yes folks, the ultrasound is certainly here to stay!

Dec 31, 2013

Iceland to the foreigner

Iceland is a country of 320.000 inhabitants known for welcoming visitors wholeheartedly. The landscape is rough yet soothing and has fostered inspiring artists such as Björk and Sigurrós and lately been attracting Hollywood’s film-makers. The wild highlands, mountains and clean water provide the world’s best raw-materials such as salmon and lamb-meat and Reykjavik is renowned for it’s high quality restaurants. The atmosphere in Iceland is unique and if you at anytime need peace from all the ongoing events you never far a way from a natural hot spring to soak in. Iceland is definitely the place to visit for the adventurer seeking something different!

More about Iceland

The 5 best hot springs in Iceland

A few selected videos from Iceland...

Dec 7, 2013

Chest pain with subtle yet serious ECG changes

Following is a classic case underlining the importance of "STEMI equivalents" or ECG patterns requiring prompt attendance and cath lab activation as if it were a true STEMI.
A 74 year-old previously healthy woman presented to the emergency department by ambulance with chest tightness and left arm numbness following exercise. She was stable on arrival, BP was 140/65 and pulse regular 65/min and pain free after receiving nitroglycerin.
Describe the T waves shown on the ECG
This ECG mainly shows prominent inverted T waves in V2-5.
What are they indicative of?
Biphasic or inverted T waves in precordial leads strongly suggest critical left anterior descending coronary artery stenosis. This pattern is referred to as Wellens syndrome or "LAD coronary T-wave syndrome". Generally, there is a history of angina and troponin levels are either normal or mildly elevated. ST elevations are rarely present. The majority of patients with this ECG pattern will develop extensive anterior myocardial infarction within weeks if no intervention is taken. Therefore, recognizing this pattern is of critical importance and cardiac catheterization should be performed promptly, despite a pain free patient.
Which test could be lethal for this patient?
This patient is likely to have very limited circulation to the anterior myocardium. A stress test could easily induce arrhythmias or in worst case cardiac arrest.
What are STEMI equivalents?
Patients with STEMI equivalents have acute coronary artery occlusion without the classic ST elevation patterns we have all been taught not to miss.
A paper by Rokos et al published in the American Heart Journal in 2010* reviewed STEMI equivalents requiring cath lab activation:
1) Posterior (V1-3) ST depressions
2) ST elevation >1mm in aVR along with depression of anterior leads
3) de Winter ST/T wave complexes anteriorly

This article is free to view in link below but our great colleague and emergency physician Andy Neill in Ireland has reviewed the article nicely on his blog.

Wellens syndrome is a chronic coronary artery occlusion and therefore not a STEMI equivalent. It is nonetheless a serious and unstable condition that requires prompt intervention and every physician should be able to recognize it.

Our patient was admitted to the cardilogy ward and was scheduled for cardiac catheterization the following day. She was stable and pain free on admission. A few hours later she developed a circulatory collapse and underwent acute catheterization which revealed critical stenosis of the left main coronary artery, LAD, circumflex artery and right coronary artery.

* IC Rokos, WJ French, A Mattu, G Nichol, ME Farkouh, J Reiffel, GW Stone. Appropriate Cardiac Cath Lab activation: Optimizing electrocardiogram interpretation and clinical decision-making for acute ST-elevation myocardial infarction. Am Heart J, 160 (2010), pp. 995–1003.

Read more about Wellens at LITFL What is Wellens syndrome?

Maria Reynisdottir (stud. med.)