part man, part machine…

the case.

48 year old male is bought to the Emergency Department via ambulance following a syncopal episode. They are unable to obtain a blood pressure & describe ‘some sort of device coming out of his chest’ !!

He has a past medical history of a severe, familial dilated cardiomyopathy (LVEF ~18-20%) & atrial fibrillation and is awaiting cardiac transplantation. Six months ago he was implanted with a left ventricular assist device.

He has recently felt systemically well, however today he reports collapsing without prior warning shortly after getting out of his chair. Following a brief loss of consciousness, he quickly returned to his normal self.

Left ventricular assist device [LVAD]

These are intricate mechanical pumps utilised in the management of end-stage cardiac failure refractory to aggressive medical therapy, typically bridging a patient to cardiac transplantation.

The first implantation of an LVAD occurred back in 1984, however their technology and success have markedly improved since then. The landmark REMATCH paper demonstrated significant survival increase [52% vs 25% at 1 year, p=0.002] with an improved quality of life. Currently over 90% of LVAD-supported patients will survive to 1 year post-implantation.

Indications.

  • Bridge to cardiac transplant.
  • Bridge to recovery – potential reversible myocardial pathology.
  • Destination therapy – long-term assistance for patients ineligible for transplant

The components.

  • Inflow cannula.
    • placed within the left-ventricle
    • draws blood from the LV into the pump.
  • The pump.
    • is located at the apex of the LV.
    • houses the impeller - a frictionless rotor which is magnetically levitated. This rotates at speeds of >3000 rpm & can generate up to 10 litres per minute of blood flow.
  • Outflow graft.
    • flexible & gel-impregnated
    • conveys blood from the pump to the ascending aorta.
  • Driveline.
    • tunneled subcutaneously from the pump & exits typically in the patients epigastrium or right-upper quadrant
    • contains wires from external controller.
  • Controller.
    • regulates power, monitors VAD performance & displays alarms,
    • displays battery life & function.
    • allows data to be downloaded for analysis.
  • Batteries.
    • at least two rechargeable lithium-ion batteries are carried at all times
    • the device is also capable of recharging on standard power supply.

What do they look like ?

Figure 2 HeartWare HVAD

HeartWare HVAD. A continuous flow device designed to draw blood from the LV & propel it through an outflow graft connected to the patient’s ascending aorta. The inflow cannula is surgically implanted into the left ventricle & blood is conveyed through the pump via an impeller at operating speeds of 2400-3200 rpm (resulting in up to 10L/min of blood flow)(Courtesy of HeartWare International Inc, Framingham, Massachusetts, USA.)

Thoratec HeartMate II. An axial-flow VAD with an impeller [the only moving part] that propels blood from the inflow cannula in the left ventricle to the ascending aorta. (Reprinted with the permission of Thoratec Corporation)

Thoratec HeartMate II. An axial-flow VAD with an impeller [the only moving part] that propels blood from the inflow cannula in the left ventricle to the ascending aorta. (Reprinted with the permission of Thoratec Corporation)

HeartWare LVAD controller. Displays battery life, impeller RPM, cardiac output & power usage. Alarms are also displayed here

HeartWare LVAD controller. Displays battery life, impeller RPM, cardiac output & power usage. Alarms are also displayed here

LVAD CXR

A typical CXR for a patient with an implanted left ventricular assist device. These patients will often have pacemakers or AICDs implanted also.

The assessment of a patient with a VAD begins like any other; a primary survey !! However, there are a few specifics we should mention.

1) BLOOD PRESSURE MEASUREMENT.

Due to diminished [& sometimes absent] peripheral pulses in the continuous-flow VADs, standard non-invasive blood pressure is difficult [perhaps impossible] to obtain.

Blood pressure can be measured with (1) a manual sphygmomanometer & (2) Doppler ultrasound over the radial or brachial artery. Cuff pressure is gradually reduced until a constant sound is heard – signifying the mean arterial pressure. Alternatively, in a critically ill patient just place an ultrasound-guided arterial line !

Radial artery Doppler [MAP]

Mean arterial pressure in patient with left ventricular assist device [LVAD]. Doppler gate through radial artery. Regular spikes indicate minor pressure augmentation from native LV function.

Radial artery doppler with falling maanual sphygmomanometer pressure. Pulse returnsa due to native LV function.

Radial artery doppler with falling manual sphygmomanometer pressure. Pulse returns due to native LV function.

Radial artery doppler with ongoing falling manual sphygmomanometer pressure approaching mean arterial pressure...

Radial artery doppler with ongoing falling manual sphygmomanometer pressure approaching mean arterial pressure…

 

 

 

 

 

 

 

In this case the patients’ mean arterial pressure was measured at 59 mmHg. He normally runs at 70-80mmHg.

2) ASSESSING DEVICE FUNCTION.

  • Check that the pump is running. Auscultate the epigastrium/precordium for a continuous noise ! This is the pump operating.
  • Check the controller for;
    • BATTERY FUNCTION !
    • Flow
    • Power etc…

3) A BEDSIDE ECHO CAN BE A VERY POWERFUL TOOL.

  • VAD malfunction can result in catastrophic consequences & marked haemodynamic instability.
  • ECHO will allow rapid assessment of RV:LV chamber size comparison.
    • Small RV: consider Hypovolaemia [check IVC also]
    • Large RV: consider Pulmonary hypertension [correct hypoxia & acidosis]
    • Large RV + LV: consider VAD-thrombus !!
  • ECHO will also allow assessment of IVC diameter & collapsibility as well as the presence of pericardial effusion ± tamponade.
    • Will also confirm the correct positioning of the inflow cannula [which can migrate or kink overtime].

Call your nearest LVAD or Cardiac-transplant centre as soon as possible for assistance in the care of these complex patients !!

Table 1 VAD-Hypotension Causes

It is important to acknowledge that these devices are

  1. preload dependent &
  2. afterload sensitive.

Any physiological or pathological influence on either of these can significantly alter pump-efficiency and result in hypotension !!

The most common adverse event with the first month of implantation. These patients have multiple reasons for bleeding…

  1. Anticoagulation: typically warfarin.
  2. Antiplatelet therapy: often dual agents.
  3. Acquired von-Willebrand syndrome:
  4. Increased incidence of AV-malformations & angiodysplasia of the gastrointestinal tract. 

Common sites of bleeding include the GIT, epistaxis, intracerebral haemorrhage & intrathoracic bleeding. Clearly most of these will be clinically obvious, but always consider occult GIT haemorrhage in the hypotensive VAD-patient.

The management of bleeding in VAD-implanted patients is a particularly challenging therapeutic dilemma. If anticoagulation-reversal is undertaken, it should be for as short a time-period as possible. You do not want them going on to have a subsequent embolic/thrombotic event !!

There are multiple case reports regarding the various therapeutic options for life-threatening haemorrhage & they include; prothrombin complex concentrates, FFP, TXA, desmopressin [defective vWF] & Factor VII.

Every VAD-patient that presents to your department should have a 12-lead ECG as soon as possible….

Both ventricular and atrial dysrhythmias are incredible common amongst patients with VADs. In fact; ventricular dysrhythmias can be surprisingly well tolerated in these patients, with multiple cases reports of very stable patients in both VT & VF !!!

Potential causes for dysrhythmias include;

  • Local trauma [VAD comes into contact with endocardium, see Suction Events below]
  • Hypovolaemia
  • Ischaemia
  • Electrolyte disturbances
  • other… [remember they have a significantly diseased myocardium to begin with]

Management options;

  • Assess volume status & ensure adequate preload. Utilise bedside ECHO…
  • Pharmacotherapy:
    • Amiodarone
    • Lignocaine
    • Procainamide
  • Electrical cardioversion is safe in these patients…
  • At your VAD centre – there may be attempts to reduce VAD-pump speed;  but this is usually performed under guidance of transoesophageal ECHO.

A result of large negative pressures within the LV created by continuous-flow LVADs. This results in the LV collapsing on itself, causing marked leftward deviation of the interventricular septum.

Causes of suction events include;

  • Right ventricular failure
  • Hypovolaemia
  • Cardiac tamponade
  • Dysrhythmias
  • Inflow cannula malposition.

Management;

  • IV fluids & maintain preload.
  • Obtain and ECG & treat dysrhythmias as above.
  • Bedside ECHO
  • Again; your VAD-centre may adjust pump-speeds.

Infections can involve any portion of the VAD including the surgical site, driveline, device pocket & the pump itself !!

Whilst Gram-positive organisms are more commonly implicated in VAD-infections, don’t forget to cover for Gram-negatives & multi-drug resistant organisms. Fungal infections have been documented also.

Culture these patients from every possible site [including exit-site swabs] & maintain a high index of suspicion for occult sepsis in VAD patients present with either hypotension or fever !

With his borderline hypotension, he was rather symptomatic with postural changes.

  • Afebrile.
  • Soft, non-tender abdomen with negative PR.

His results were largely unexciting…

  • Normal haemoglobin.
  • Electrolytes & renal function normal for him.
  • INR 2.4. PLTs 264.
  • Inflammatory markers unremarkable. WCC 8, CRP 14.
  • 12-lead ECG: atrial sensing, ventricular pacing.
    • No episodes of dysrhythmia whilst on telemetry.
  • CXR [seen above].

Here is his bedside ECHO…

PLAX view. Inflow cannula visible in LV-apex. Small RV. No pericardial effusion.

 

Marked respiratory collapse of the inferior vena cava suggesting volume depletion.

Our patient was treated with two small fluid boluses [250mLs of saline] which improved his mean pressure to 74mmHg. At this stage he was admitted under Cardiology to ‘fine-tune’ his medications…

  1. Partyka, C., & Taylor, B. (2014). Review article: Ventricular assist devices in the emergency department. Emergency Medicine Australasia, 26(2), 104–112. doi:10.1111/1742-6723.12171

I acknowledge that my paper is not Free Open Access; hence why I have put this post together. I am however able [& very keen] to email you a copy upon your request.

So, email me at chrispartyka@gmail.com & you’ll get your copy !!

two in two days…

I have recently prepared a lecture on a current, yet still controversial topic for work following exposure to these two interesting cases. Here are the cases & their discussion as well as the slide-show attached… 

case one.

a 74 year old male presents to ED following a syncopal episode at home. He apparently collapsed without warning whilst taking the rubbish outside.

With the paramedics, he is alert & oriented but has a pulse of 120 per min and a systolic blood pressure of 70mmHg. His prehospital ECG demonstrates a right bundle branch block that resolves prior to ED arrival.

He arrives to ED in extremis. He is agitated, hypoxic [SaO2 92% on 15L NRB, RR 32, clear chest] & shocked [P 124, BP 72/50, cold & mottled]. Whilst his GCS is 13, he has no focal neurological signs. His blood glucose & temperature are normal.

Before you continue. Pause to consider the potential diagnoses. How are you going to differentiate these further ??

massive PE cxr

Venous blood gas - metabolic [lactic] acidosis

Venous blood gas – metabolic [lactic] acidosis with impaired renal function.

Initial resuscitation.

  • High-flow oxygen via non-rebreather mask
  • 2x large-bore IV-access
  • Empiric fluid bolus

Differential diagnoses.

  • Undifferentiated shock [cardiogenic vs septic vs obstructive...]
    • ?AMI
    • ?AAA
    • ?Aortic dissection
    • ?Haemorrhage
    • ??sepsis, others….

You take your ultrasound to the bedside…

http://www.youtube.com/watch?v=P2bfuvh5v4E

Massively dilated right ventricle with visualisation of blood clot 'in transit' through the right atrium.

Massively dilated right ventricle with visualisation of blood clot ‘in transit’ through the right atrium.

These findings on the RUSH exam allowed us to make the provisional diagnosis of massive pulmonary embolism with obstructive shock !

Unfortunately, soon after the diagnosis is made the patient deteriorates and has a PEA arrest. The decision is made to threat with empiric thrombolysis with alteplase.

There is a protracted period of resuscitation with periods of spontaneous circulation interspersed  with short bursts of CPR. Despite an ongoing, escalating adrenaline requirement he was safely [eventually] transferred to Intensive Care.

Unfortunately, he has a further PEA arrest and subsequently asystole some 7 hours after arriving to ED and could not be resuscitated.

THROMBOLYSIS FOR PULMONARY EMBOLISM

Here are the slides from my presentation looking at the evidence & potential roles for thrombolysis for pulmonary embolism.

 

case two – precisely 24 hours later….

a 47 year old female is bought to ED following a pre-hospital notification regarding her ‘life-threatening asthma’.

She was found by paramedics to have significant respiratory distress & profound hypoxia, so administered intramuscular adrenaline [500mcg x2] plus continuous salbutamol whilst transporting her to ED.

Upon arrival she is alert with a patent airway, but profound tachypnoea & hypoxia [RR 44, SaO2 92% 15L NRB]. Surprisingly she has a clear chest with good air-entry. There are no wheezes or crackles. She is tachycardic but normotensive [P 124/min, BP 118/70], with warm peripheries.

You cannot help but notice she has a “Cam boot” on her right foot. She sustained an undisplaced Weber B fracture 3 weeks earlier, which has been managed conservatively.

Again, pause to consider the potential diagnoses. How are you going to differentiate these further ??

ecg1

CXR01

Submassive ABG#1

A-a gradient of ~580… 

Initial resuscitation.

  • BiPAP initiated for oxygen requirement & work of breathing.
  • IV access & empiric fluid bolus
  • Heparin bolus + infusion based on presence of cam-boot & potential for DVT/PE
  • Empiric IV ABx given; atypical presentation.

Differential diagnoses.

  • Pulmonary embolism
  • ?Asthma – less & less likely…
  • ?Infectious
  • ?Metabolic

You take your ultrasound to the bedside…

http://www.youtube.com/watch?v=Re-RU6CQ-AY

Our concerns…

PE-ECHO

With these findings, our predominate concern was for submassive pulmonary embolism.

It is acknowledged that further investigation (ie. CTPA) was impossible without intubation & mechanical ventilation due to profound oxygen requirement and inability to lay-flat.

A decision is made for RSI, which takes place without issue.

Here is her CTPA…

http://www.youtube.com/watch?v=GZQUqCpzxeg

Now ask yourself….
Are you going to use thrombolysis on this patient ?!?!

It is decided given her oxygen requirement, age and clot-burden to proceed to thrombolysis. She receives 100mg of alteplase over two hours.

The following morning she is extubated without issue [ie. normal gas-exchange] & is discharged home on Day 5 !!

This is her discharge ECHO…

ECHO on DC

  • Consider massive & submassive PE as a cause for undifferentiated shock.
  • Have a low threshold to investigate these patients yourself with a bedside ECHO [ie. specifically, RUSH exam, extension of BLUE protocol].
    • Includes undifferentiated shock or unexplained dyspnoea/hypoxia.
  • ECHO specifics to examine include:
    • RV size [esp. RV:LV ratio]
    • RV contractility ?hypokinesis.
    • Paradoxical septal motion [ie. flattening or leftward bowing]
    • McConnell’s sign - right ventricular free wall hypokinesis with apical sparing.
    • Tricuspid regurgitation.
  • Consider thrombolysis in:
    • Massive PE
    • Presumed massive PE with PEA arrest/shock
    • Submassive PE:
      • Profound RV dysfunction [abnormal ECHO + positive troponin]
      • Severe hypoxaemia/oxygen requirement
      • Age < 75
  • Consider contraindications carefully

Contraindications to Thrombolysis

  • Remember there are other alternatives:
    • Interventional radiology
    • Cardiothoracic surgery

Literature.

  • Goldhaber SZ, Visani L, De Rosa M, et al. for ICOPER. Acute pulmonary embolism; clinical outcomes in the International Cooperative Pulmonary Embolism Registry. Lancet 1999;353:1386-1389
  • Grifoni, S., Vanni, S., Magazzini, S., Olivotto, I., Conti, A., Zanobetti, M., et al. (2006). Association of persistent right ventricular dysfunction at hospital discharge after acute pulmonary embolism with recurrent thromboembolic events. Archives of internal medicine, 166(19), 2151–2156. doi:10.1001/archinte.166.19.2151
  • Kline, J. A. (2009). Prospective Evaluation of Right Ventricular Function and Functional Status 6 Months After Acute Submassive Pulmonary Embolism. Chest, 136(5), 1202. doi:10.1378/chest.08-2988
  • Frémont, B. (2008). Prognostic Value of Echocardiographic Right/Left Ventricular End-Diastolic Diameter Ratio in Patients With Acute Pulmonary Embolism *. Chest, 133(2), 358. doi:10.1378/chest.07-1231
  • Böttiger, B. W., et al. (2008). Thrombolysis during resuscitation for out-of-hospital cardiac arrest. The New England journal of medicine, 359(25), 2651–2662.
  • British Thoracic Society Standards of Care Committee Pulmonary Embolism Guideline Development Group. (2003, June). British Thoracic Society guidelines for the management of suspected acute pulmonary embolism. Thorax.
  • Jaff, M. R., Mcmurtry, M. S., Archer, S. L., Cushman, M., Goldenberg, N., Goldhaber, S. Z., et al. (2011). Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension: A Scientific Statement From the American Heart Association. Circulation, 123(16), 1788–1830. doi:10.1161/CIR.0b013e318214914f
  • Konstantinides, S., et al. Management Strategies and Prognosis of Pulmonary Embolism-3 Trial Investigators. (2002). Heparin plus alteplase compared with heparin alone in patients with submassive pulmonary embolism. The New England journal of medicine, 347(15), 1143–1150.
  • MD, M. S., PhD, C. B., DO, L. S., MD, F. R., DMD, M. M., & Investigators, M. (2013). Moderate Pulmonary Embolism Treated With Thrombolysis (from the “MOPETT“” Trial). The American Journal of Cardiology, 111(2), 273–277.
  • Steering Committee. (2012). Single-bolus tenecteplase plus heparin compared with heparin alone for normotensive patients with acute pulmonary embolism who have evidence of right ventricular dysfunction and myocardial injury: rationale and design of the Pulmonary Embolism Thrombolysis (PEITHO) trial. American Heart Journal, 163(1), 33–38.e1.
  • Sharifi, M., Bay, C., Schwartz, F., & Skrocki, L. (2014). Safe-dose thrombolysis plus rivaroxaban for moderate and severe pulmonary embolism: drip, drug, and discharge. Clinical cardiology, 37(2), 78–82. doi:10.1002/clc.22216
  • PEITHO RESULTS (slideshow) via ClinicTrialResults.org
  • MD, S. D., RN, P. M., BA, L. R., RDMS, M. L. M., MPH, J. R.-S., MPH, S. B., et al. (2014). Right Ventricular Dilatation on Bedside Echocardiography Performed by Emergency Physicians Aids in the Diagnosis of Pulmonary Embolism. Annals of Emergency Medicine, 63(1), 16–24. doi:10.1016/j.annemergmed.2013.08.016

Social Media covering Thrombolysis for Pulmonary Embolism.

a whack to the flank….

the case.

an 84 year old man is bought to your emergency department following a 3 metre fall from a ladder. He has landed on his right-hand side & is complaining of severe bilateral chest & flank pain.

His systolic blood pressure with the paramedics has been 100-105 mmHg, except for a transient episode of hypotension [72mmHg systolic] which resolved after a 300mL  bolus of crystalloid. On arrival to ED he has a GCS of 15,  full recollections of events & no focal neurological deficit but is in excruciating pain.

Pulse 66/min. BP 106/72. SaO2 94%. RR 26.

He is on warfarin for atrial fibrillation, but does not recall his last INR measurement.

  • Rapid assessment [Primary survey] & concomitant treatment of life threatening injuries.
    • Multidisciplinary approach. Trauma call. Resuscitation bay.
    • Includes empiric C-spine immobilisation [mechanism, age, distracting injuries]
  • Rapid detection of early evidence of haemorrhage.
    • E-FAST.
    • Pelvic x-ray.
    • Early CT-scan including arterial-phase if remains ‘stable’.
  • Preparation for massive transfusion.
    • Multiple possible injuries each with potential for massive blood loss.
    • Minimum of 2x large-bore cannula.
    • Cross-matched blood.
  • Analgesia.
    • Titrated intravenous opiates.
    • Likely to require PCA.
  • Preparation/expectation for warfarin reversal.
    • Prothrombinex.
    • Vitamin K.
    • Fresh frozen plasma.
    • Consideration of tranexamic acid if requiring massive transfusion.
  • Assess for potential medical reasons for ‘fall’.
    • ie. was this syncope ?
    • ECG
  • Seek and treat less significant traumatic injuries.
    • Secondary survey.
    • CT-Brain + C-spine.
    • X-rays dictated by physical exam.
  • Others:
    • Family notification.
    • Consider tetanus booster + prophylactic antibiotics.

Whilst the team are seeing to the primary survey & getting IV access, you obtain the following images on your bedside FAST exam…

RUQ view

RUQ view

http://www.youtube.com/watch?v=MyD8ctITRfQ

http://www.youtube.com/watch?v=GY2WqvbhZvc

Moderate amount of hypoechoic material in the RUQ ?blood+clot. This appears to be more in the perinephric space than ‘Morrison’s pouch’.

The remainder of the E-FAST is unremarkable.

The patient remains haemodynamically stable, however receives empiric reversal of his anticoagulation with 50IU/kg of prothrombin complex concentrates [Prothrombinex®], plus 10mg IV vitamin K. He is then taken rapidly to CT for further assessment….

http://www.youtube.com/watch?v=P6OVxUYIdqE

Other positive findings included:

  • Multiple rib fractures including left sided flail segment.
  • Associated left pulmonary contusion.
  • Fractures of T4 & T8.
  • Comminuted fracture of right ilium plus left superior & inferior pubic rami.
  • Right sacroiliac joint subluxation.

RENAL TRAUMA.

  • Present in 8-10% abdominal trauma.
    • Penetrating vs Blunt mechanisms
  • Accounts for < 0.1% of trauma deaths.
  • Rarely occurs in isolation.
    • > 80% have additional visceral/skeletal injuries.
    • Often non-urological injuries result in haemodynamic instability.
  • Recall: the kidneys receive 20-25% of cardiac output [~1200mL per minute], therefore have potential for massive blood loss.

INVESTIGATIONS.

Urinalysis.

  • No correlation between presence & absence of haematuria with severity of injury.
    • ~14% of major injuries [& ~10% of minor injuries] have no haematuria.
  • No correlation between degree of microscopic haematuria and severity of injury.
  • Gross haematuria MAY correlate with severe renal injury.
    • Can miss up to two-thirds of renal injuries if used in isolation.

Ultrasound [FAST].

  • High sensitivity & specificity for free-fluid.
  • Misses up to 78% of known renal injuries.
  • Will not identify renal vascular injury.

Indications for Imaging [suspected renal injury]

Advanced imaging.
Goals of imaging are to stage the injury, assess for preexisting renal pathology, functionality/disease-state of contralateral kidney & assess for concomitant traumatic injuries.

  • CT with IV contrast.
    • GOLD STANDARD.
    • Delineates grade of injury [contusion, laceration, haematoma] + perfusion abnormalities.
    • Contrast extravasation = active haemorrhage.
    • Use of delayed scan [~10min post contrast administration] = ?urinary extravasation.
  • IV urography.
    • KUB-xray is taken ~10 minutes after an IV contrast bolus is administered.
    • ↓ Sn in hypotensive/shocked patients.
    • Does not aid in grading.
    • Does have a role in on-table imaging if patient is taken straight to laparotomy for other reasons.
  • Formal angiography.
    • Allows for embolisation or stenting at initial assessment.
    • Has role for further assessment for delayed injuries/pathology [ie. thrombosis, aneurysm formation].

GRADING OF RENAL INJURIES.

Grading of Traumatic Renal Injury

screenshot656

Schematics of Renal Injury grades ~ Courtesy of onsurg.com

For further examples of renal injuries check out Radiopaedia.org

TREATMENT.

  • Standard ‘Trauma-rules’ apply.
    • Haemodynamic compromise → exploratory laparotomy.
  • Majority of renal injuries [Grades I, II & III] can/will be managed conservatively.
    • Some Grade IV injuries will too.
    • Only ~9% of renal injuries require surgical exploration. Of these ~11% require nephrectomy.
  • Indications for surgical intervention.
    • Life-threatening haemorrhage.
    • Expanding, pulsatile or non-contained retroperitoneal haematoma.
    • Renal avulsion injury [Grade V]
    • Renal pelvis or ureteric injuries DO require repair. Urinary extravasation is NOT a sole reason for exploration. These usually resolve spontaneously.
  • Some injuries are amenable to stenting or angio-embolisation.

COMPLICATIONS.

  • Delayed bleeding
    • usually secondary to AV-fistula formation [~25% of Grade III or IV injuries]
  • Urinary extravasation
  • Urinoma
  • Perinephric abscess
  • HTN

DISPOSITION.

  • The majority of patients will require admission for concomitant injuries.
  • Patients with gross haematuria should be admitted & observed until it clears.
  • Who can be discharged ?
    • Patients with microscopic haematuria & no indications for imaging.
    • Light duties only & close follow-up.

  1. Rosenʼs Emergency Medicine. Concepts and Clinical Approach. 7th Edition
  2. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition.
  3. Renal Trauma – Trauma.org
  4. Renal Trauma Grading – Radiopaedia.org

pupils predict pathology…

the case.

A 34 year old male is bought to your ED with reduced level of consciousness. He was at a restaurant having dinner with family & friends when he excused himself to use the bathroom. They found him 15 minutes later slumped near the toilet – unconscious and barely breathing.

On arrival to ED, he is GCS 3 with pinpoint pupils. He has already received 2mg of naloxone by paramedics without affect.

Coma & Pin-Point Pupils.

  • Neurological.
    • Pontine stroke.
      • Infarction
      • Haemorrhage
  • Toxicological.
    • Opiates
    • Clonidine
    • Barbiturates
    • Gamma-hydroxybutyrate [GHB]
    • Cholinergics.
      • organophosphates, carbamates
      • nerve gas
      • mushrooms
    • Chloral hydrate
    • Phenothiazines
    • Atypical antipsychotics
      • Olanzapine, quetiapine, clozapine
  • Encephalopathy

Of course, some of these toxidromes will have associated features that will make them more or less likely given this limited clinical information.

After securing the airway, you transfer the patient to radiology for a non-contrast CT-brain….

Massive-type pontine haemorrhage.

Massive-type pontine haemorrhage.

Pontine Haemorrhage

Primary pontine haemorrhages are rare and account for only 5-10% of intracranial haemorrhages.

They are one of the classic locations for hypertensive intracerebral haemorrhages [along with the putamen, thalamus and cerebellum].

Other risk factors include;

  • Vascular malformations [cavernous or arteriovenous]
  • Anticoagulation
  • Sympathomimetic abuse [esp. cocaine]
  • Tumours [primary or metastatic]
  • Smoking

Clinically;

  • Severe disturbances of consciousness
    • Abrupt and severe
    • Stupor → coma !
  • Oculomotor disturbances
    • Pin-point pupils
    • plus other cranial nerve findings
  • Tetraparesis
  • Respiratory failure

Management;

  • Aggressive, upfront neuro-resuscitation.
    • Secure airway [tape the tube, don't tie]
    • Adequate sedation post-intubation
    • Avoid hypoxia & hypotension
    • Avoid excessive PEEP
    • Glucose control
  • Neurosurgical.
    • Open clot evacuation is typically avoided.
    • Stereotactic haematoma aspiration may be offered.

Prognosis;

  • Generally very poor & often fatal.
  • Often fatal in the setting of hypertensive haemorrhage
  • Predictors of poor outcome include:
    • Coma on admission
    • Intraventricular extension of haemorrhage
    • Acute hydrocephalus

  1. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition.
  2. Murray L, Daly F, Little M & Cadogan M. Toxicology Handbook. 2nd Edition. Elsevier 2011
  3. Goto, N et al. Primary pontine hemorrhage: clinicopathological correlations. Stroke. 1980;11:84-90
  4. Shin, SC et al. Primary Pontine Hemorrhage. An Analysis of 35 Cases and Research in Prognostic Factors. Kor J Cerebrovascular Surgery. 2007: 9:41-5.
  5. Wessels T, et al. CT Findings and Clinical Features as Markers for Patient Outcome in Primary Pontine Hemorrhage. AJNR Am J Neuroradiol 25:257–260
  6. Nishizaki, T et al. Factors Determining the Outcome of Pontine Hemorrhage in the Absence of Surgical Intervention. Open Journal of Modern Neurosurgery, Vol. 2 No. 2, 2012, pp. 17-20
  7. Coma & small pupils – LITFL.com
  8. Pontine Haemorrhage at Radiopaedia.org 

chest pain and…

the case.

a 41 year old male presents with sudden severe retrosternal chest pain radiating into the right flank.

He also reports 3-4 weeks of intermittent chest tightness & that his doctor told him he “may need a heart valve fixed one day”.

This is his ECG.

AS+LVH

  • Rate.
    • 66 bpm.
  • Rhythm.
    • Regular, sinus.
  • Axis.
    • Normal [~ 27*]
  • Intervals.
    • PR ~ 160 msec
    • QRS ~ 100 msec
    • QTc ~ 375 msec
  • Segments.
    • STE (V2-3) ?BER vs appropriate discordance
    • STD (lead III only) ~1/2mm
    • TWI (III only), plus T-wave flattening in aVF.
  • Others.
    • Non-specific intraventricular conduction delay
    • LVH by voltage-criteria;
      • S(V2) + R(V5) > 45mm
      • No strain pattern

Interpretation.

Sinus rhythm with left ventricular hypertrophy (by voltage-criteria).

This is his bedside ECHO.

http://www.youtube.com/watch?v=Ki9kYPQhByk

http://www.youtube.com/watch?v=d8UHXwx3Wk0

LV hypertrophy visible on the parasternal long-axis and a large aortic regurgitant jet seen on the apical four chamber.

Aortic Dissection.

” There is no disease more conductive to clinical humility than aneurysm of the aorta. ”
- Sir William Osler.

When it comes to aortic dissection, maintaining a high index of suspicion is crucial. Whilst it does not always present in the classical ‘chest pain and…” manner described in textbooks, it is important to keep in mind the risk factors associated with the disease as well as the pertinent features of history, examination and imaging that may lead us to pursue the diagnosis more aggressively.

Traditional risk factors:

  • Chronic hypertension
  • Bicuspid aortic valve + other congenital cardiac disease
  • Coarctation
  • Atherosclerosis
  • Marfan or Ehlers-Danlos syndrome
  • Vasculitis [SLE, syphilis, GCA etc.]
  • Prior instrumentation [CABG, valve surgery, IABP]

History.
Note that most episodes of chest pain are acute and severe. Do not rely on migration, radiation etc. Pain can still be atypical.

Ao Dissection

Physical examination.
Note that the classic pulse deficits and murmur of aortic insufficiency are not always present !!

Ao Dissection

Basic investigations.

Ao Dissection

It is important to remember the list of abnormal CXR findings which include;

  • widened mediastinum
  • abnormal aortic contour including loss of aortopulmonary window
  • aortic ‘double-calcium’ sign
  • pleural effusion
  • left apical cap
  • tracheal deviation
  • depressed left bronchus
  • rightward deviation of nasogastric tube
Left apical cap - Courtesy of crashingpatient.com

Left apical cap – Courtesy of crashingpatient.com

Double calcium sign - courtesy of wikiradiography.com

Double calcium sign – courtesy of wikiradiography.com

Widened mediastinum - sometimes its quite straight forward

Widened mediastinum – sometimes it’s quite straight forward

Advanced imaging.

  • CT-aortogram:
    • Ideally the next best test.
    • Confirm the diagnosis, but also demonstrates the extent of the disease & identifies complications.
      • If negative for dissection, may identify alternate pathology.
    • Rapid.
    • Geographically not ideal. Must leave resuscitation bay !!
    • Sn 100% [96-100], Sp 98% [87-99]

Type A Aortic Dissection

  • Transoesophageal ECHO:
    • Operator dependent may also be an appropriate test.
    • Consider use in unstable patient & transfer out of ED is not feasible or safe.
    • Identifies AR as well as pericardial effusion ± tamponade.
    • Limited visualisation of arch branches and distal ascending aorta.
    • Sn 98 [95-99], Sp 95% [92-97]
  • MRI:
    • No radiation
    • Geographically isolated & takes time [>30mins]
    • Limited availability
    • Sn 98 [95-99], Sp 98 [95-100]

Management.

  • Analgesia
    • May help with anxiolysis and blood pressure control
  • Ensure adequate IV access & be equipped for massive transfusion
    • Cross-match & notify blood-bank
    • Fluid warmer, rapid-infuser prepped
  • Aggressive blood pressure control
    • Goal is to minimise shear stress on the intimal flap.
    • Invasive monitoring [arterial line]
    • First line – beta-blockers:
      • Esmolol infusion
      • Metoprolol boluses
      • Labetalol
      • Target: Pulse 60-80 bpm
    • Second line - vasodilators [ensure adequate rate-control first, to avoid rebound tachycardia]
      • Nitrates [GTN infusion]
      • Sodium nitroprusside
      • Nicardipine
      • Target: SBP < 120 mmHg
  • Assess for complications.
    • Rupture
    • Tamponade
    • Cardiac ischaemia secondary to dissection in RCA [0.1-0.2% of all STEMIs]
    • End-organ ischaemia
      • Brain [Stroke symptoms]
      • Limbs
      • Bowel
      • Kidneys
      • Spine [paralysis]
  • Urgent surgical consultation
    • Surgery for Type A dissection, those with ongoing pain, aortic branch occlusion, evidence of leak on CT or development of local aneurysms.
  • Notify anaesthetics and intensive care of potential incoming patient.

With chest pain radiating into abdomen & flank and an ECHO demonstrating aortic regurgitation, our patient was sent to radiology for a CT-Aortogram.

Fortunately, this excluded dissection but did demonstrate aneurysmal dilatation of the ascending aorta [to 46mm].

His formal ECHO reported moderately dilated LV w/ mild concentric hypertrophy & normal systolic function. Bicuspid aortic valve with mild-moderate stenosis & moderate regurgitation.

He has discharged home after exclusion of atypical acute coronary syndrome with a referred for outpatient surgical management of his valvular disease.

  1. Rosenʼs Emergency Medicine. Concepts and Clinical Approach. 7th Edition
  2. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition.
  3. Hagan, P. G., Nienaber, C. A., Isselbacher, E. M., et al. (2000). The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA: the journal of the American Medical Association, 283(7), 897–903.
  4. Klompas, M. (2002). Does this patient have an acute thoracic aortic dissection? JAMA: the journal of the American Medical Association, 287(17), 2262–2272.
  5. Upadhye S, Schiff K. Acute aortic dissection in the emergency department: diagnostic challenges and evidence-based management. Emerg Med Clin North Am. 2012 May;30(2):307-27

having a dig…

the case.

87 year old female presents to your ED following an intentional overdose. She tells you that approximately 4 hours ago she ingested ‘most of [her] digoxin tablets’ that she bought earlier in the afternoon.

After speaking to family and paramedic staff, in reality, she has systematically dissolved and swallowed close to 150 tablets of 62.5mcg digoxin; ~ 9.4 milligrams !!

Acute intoxication  occurs with >10x the normal daily dose ingested.
Typically 75mcg/kg in children is safe.

Potentially lethal digoxin toxicity can be predicted by:

  1. Dose ingested >10mg in adults [>4mg in children]
  2. Serum digoxin level > 15 nmol/L at anytime
  3. Serum potassium > 5.5 mmol/L

  • VBG.
    • pH 7.31 / pCO2 54 / HCO3 26 / BE 1 / Lactate 2.8
  • BSL.
    • 6.1 mmol/L
  • Potassium [from blood gas].
    • 4.7 mmol/L
  • 12-lead ECG.

Dig Overdose

  • Rate.
    • ~54 /min
  • Rhythm.
    • Irregular
    • No discernible P-waves
  • Axis.
    • Normal [+90*]
  • Intervals.
    • PR – n/a
    • QRS ~ 80-90msec
    • QTc ~ 380 msec
  • Segments.
    • Down-sloping ST depression in leads V5-V6.
  • Other.
    • Incomplete LBBB pattern
    • Movement artefact [most pronounced in lead I & III]

Interpretation.
Slow atrial fibrillation with lateral ST changes consistent with digoxin-effect.

The ECG manifestations of digoxin toxicity centre around two electrocardiographic effects;
(1) increased automaticity & (2) AV-blockade.

  • Increased automaticity
    • Ventricular ectopy, bigeminy or trigeminy.
    • SVTs with AV-block [atrial flutter or atrial tachycardia]
  • AV blockade
    • 1st, 2nd or 3rd degree AV-block
    • Atrial fibrillation with ventricular response < 60 bpm

The other ‘classic’ ECG for dig-toxicty is bidirectional ventricular tachycardia [often found on exams...]

  • Hallmark is beat-to-beat alternation of the frontal QRS axis.
    • This may manifest with alternating left & right bundle-branch blocks…

Bidirectional ventricular tachycardia – courtesy of the LITFL ECG Library

For more ECG examples check out LITFL’s ECG Features of Digoxin Toxicity.

Her level comes back at 14.5 nmol/L [Normal = 0.6-1.2 nmol/L]

Acute Digoxin Toxicity

This is a potentially life-threatening toxicology emergency & requires full cardiorespiratory monitoring and 1:1 nursing in a resuscitation area.

RESUSCITATION. 

Predict & prepare for potential life-threats;

  1. Hypotension
    • IV access x2
    • Crystalloid boluses
    • Vasopressors
  2. Cardiac dysrhythmias
    • Lignocaine 1mg/kg  [up to 100mg] IV
    • Phenytoin  15-20mg/kg [up to 1g] IV → may enhance AV-conduction
    • MgSO4 → 2-4 grams IV
  3. Cardiac arrest
    • ACLS
    • Empiric  20 ampoules of Digoxin-immune Fab [Digibind]
    • Continue resuscitative efforts for at least 30mins post-Digibind administration

Other complications & considerations;

  • Hyperkalaemia
    • NaHCO3 100mmol IV bolus [1mmol/kg in children]
    • Insulin + Dextrose
    • Calcium is still controversial !!
      • Theoretical concern regarding “Stone Heart” – calcium tetany produced by increasing the already elevated intracellular calcium levels produced by digoxin.
      • Levine M et al (2011) – 23 patients with acute digoxin toxicity received IV calcium. No increase in mortality or dysrhythmias.
  • AV-blockade
    • Atropine 600mcg IV x3 doses
    • Pacing: external or transvenous – rarely effective

DECONTAMINATION.

  • Consider activated charcoal in cooperative adults within the first hour of ingestion.
  • Caution in those with vomiting & potential co-ingestion that will lead to altered level of consciousness.

THE ANTIDOTE.

Digoxin-immune Fab [aka. Digibind]
The definitive treatment for acute digoxin poisoning !!

Indications.

  • ACUTE:
    • Cardiac arrest
    • Life-threatening cardiac dysrhythmia
    • Dose ingested >10mg in adults [>4mg in children]
    • Serum digoxin level > 15 nmol/L at anytime
    • Serum potassium > 5.5 mmol/L

THE DOSE in ACUTE DIGOXIN OVERDOSE.
No. of Ampoules = Ingested dose (mg) x 0.8 (bioavail) x 2

What if the dose is unknown ??
5 amps if patient is stable, or 10 amps if unstable.
a further 5 amp boluse can be given until stability is achieved !!

The end-point.
Restoration of normal cardiac rhythm / conduction.

Given the patients age & rapid onset of a bradydysrhythmia with associated hypotension; we decide to administer the Digibind.

At the end of 12 ampoules, her haemodynamics improve & she is taken off to Intensive Care. It is here that someone repeats her Digoxin level…

23.3 nmol/L !!!

But why ?!?! How ?!?! Didn’t we treat this ?!?!
Remember: Digoxin-assays measure both free & Fab-bound digoxin !!

  1. Murray L, Daly F, Little M & Cadogan M. Toxicology Handbook. 2nd Edition. Elsevier 2011.
  2. Rosenʼs Emergency Medicine. Concepts and Clinical Approach. 7th Edition
  3. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition.
  4. Heart of Stone?: calcium and digoxin toxicity by ThePoisonReview
  5. Levine M et al. The effects of intravenous calcium in patients with digoxin toxicity. J Emerg Med. 2011 Jan;40(1):41-6.