When Concussion Hits

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A 24 year old goalkeeper playing in the Champions League final in Ukraine is hit in the head by an opponent.  Later he makes two errors costing his side two goals.  His team lose 3-1.  5 days later he is diagnosed with having a concussion.  There is later speculation about whether this concussion caused his errors.  

Before we go on there has also been some interesting discussion on human factors including this article in The Times on focus and how too much can affect our performance.

What is concussion?

Concussion is usually used to describe a mild traumatic brain injury particularly the signs and symptoms an individual may experience after a mild traumatic brain injury.  Mild TBI is described as a GCS of 13-15 following a head injury.  

NHS UK list the following as symptoms of a concussion (1):

  • a headache that doesn't go away or isn't relieved with painkillers 
  • dizziness
  • nausea or vomiting
  • feeling stunned, dazed or confused
  • memory loss – you may not remember what happened before or after the injury 
  • clumsiness or trouble with balance 
  • unusual behaviour – you may become irritated easily or have sudden mood swings 
  • changes in your vision – such as blurred vision,  double vision or "seeing stars" 
  • being knocked out or struggling to stay awake

Most cases of concussion are mild (2) with contact sports having a relatively high incidence (3).

Concussion is believed to be caused by a functional rather than structural deficit following the brain hitting against the hard bony walls of the skull (4).

The diagnosis of concussion involves a full history and examination. Even so, over 80% of sufferers may not recognise their condition (5). 

There are a number of diagnostic tools designed to help recognising concussion none are designed to rule out concussion and neither are superior to clinical examination and history taking (6). 

It is important to remember the NICE CT Head criteria CG176.  Check out our Adult Head Injury episode.  Concussion should be diagnosed only if there is no suspicion of serious head injury or it has been ruled out with imaging.  

Concussion advice

The Charity Headway recommend the following for anyone diagnosed with concussion: 

  • Do make sure you stay within reach of a telephone and medical help
  • Do have plenty of rest and avoid stressful situations  Do show this booklet to a friend or family member who can monitor your condition
  • Do take painkillers such as paracetamol for headache
  • Don’t stay at home alone for 48 hours after leaving hospital
  • Don’t drink alcohol until you feel better
  • Don’t take aspirin or sleeping tablets without consulting your doctor
  • Don’t return to work until you feel ready
  • Don’t play any contact sport for at least three weeks without consulting your doctor
  • Don’t drive until you feel you have recovered. If in doubt consult your doctor 

Headway have an excellent booklet which you can find here

Post-concussion syndrome (PCS) is a symptom complex that includes headache, dizziness, neuropsychiatric symptoms, and cognitive impairment (7).  It affects 30-80% of patients with mild TBI.  Most cases resolve within 3 months.  MRI Brain should be used in prolonged cases to rule out more sinister causes.  Most clinicians will treat patients with PCS symptomatically (8).

Learning Points

  1. Concussion is a functional deficit following mild traumatic brain injury which is common
  2. There are many different symptoms of concussion which patients need to be advised about; diagnosis is through history and examination; no diagnostic score can be used to rule out concussion
  3. Post-concussion syndrome is vague and usually resolves within 3 months 

References

(1) https://www.nhs.uk/conditions/concussion/

(2) Vos PE, Battistin L, Birbamer G, Gerstenbrand F, Potapov A, Prevec T, Stepan ChA, Traubner P, Twijnstra A, Vecsei L, von Wild K, European Federation of Neurological Societies; EFNS guideline on mild traumatic brain injury: report of an EFNS task force; Eur J Neurol. 2002;9(3):207

(3) Guerriero RM, Proctor MR, Mannix R, Meehan WP 3rd; Epidemiology, trends, assessment and management of sport-related concussion in United States high schools; Curr Opin Pediatr. 2012 Dec;24(6):696-701

(4) McCrory P, Meeuwisse WH, Aubry M, Cantu B, Dvorák J, Echemendia RJ, Engebretsen L, Johnston K, Kutcher JS, Raftery M, Sills A, Benson BW, Davis GA, Ellenbogen RG, Guskiewicz K, Herring SA, Iverson GL, Jordan BD, Kissick J, McCrea M, McIntosh AS, Maddocks D, Makdissi M, Purcell L, Putukian M, Schneider K, Tator CH, Turner M; Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012; Br J Sports Med. 2013;47(5):250

(5) Delaney JS, Abuzeyad F, Correa JA, Foxford R; Recognition and characteristics of concussions in the emergency department population; J Emerg Med. 2005;29(2):189

(6) Giza CC, Kutcher JS, Ashwal S, Barth J, Getchius TS, Gioia GA, Gronseth GS, Guskiewicz K, Mandel S, Manley G, McKeag DB, Thurman DJ, Zafonte R; Summary of evidence-based guideline update: evaluation and management of concussion in sports: report of the Guideline Development Subcommittee of the American Academy of Neurology; Neurology. 2013;80(24):2250. Epub 2013 Mar 18

(7) Bazarian JJ, Wong T, Harris M, Leahey N, Mookerjee S, Dombovy M; Epidemiology and predictors of post-concussive syndrome after minor head injury in an emergency population; Brain Inj. 1999;13(3):173

(8) Evans RW, Evans RI, Sharp MJ; The physician survey on the post-concussion and whiplash syndromes; Headache. 1994;34(5):268

 

 

 

 

Mo Salah Mo Problems - The ACJ

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A 26 year old footballer was thrown to the ground during a football match in Kiev.  After trying to play on he has to be substituted with a shoulder injury.  One day later he is diagnosed with an acromioclavicular joint sprain. 

Anatomy of the ACJ:

From Gray's anatomy 

The acromioclavicular joint (ACJ) unites the distal clavicle and the acromion of the scapula. It contains an intra-articular disc, a synovial membrane, and articular cartilage that cover the distal end of the clavicle and the opposing surface of the acromion. (1) By the age of 40, most patients have narrowing of the joint space and possibly other degenerative findings. (2)

Examination:

Direct palpation that elicits focal tenderness at the joint is a sensitive but nonspecific finding. (3)

No specific test has proven diagnostic accuracy. (4)

But if there is no pain on direct palpation of the ACJ injury is unlikely.  

Palpation of the ACJ. Courtesy of Scott Koehler, MD.

Here is the Geeky Medic video on Shoulder examination:

(Don't forget our podcast on shoulder examination)

Injuries to the ACJ:

Injuries to the ACJ are graded with the Rockwood Classification I-VI depending on how much disruption there is the ACJ

Rockwood I means minimal disruption and so sprain would be diagnosed.  This can be managed conservatively with a sling

For more information on the Rockwood classification visit Orthobullets

Radiopaedia have an excellent article on the ACJ; here are their examples of a normal ACJ on radiograph.  

Learning Points:

  1. There is no definite test for ACJ injury and a full history and examination must be performed but if there is no tenderness on direct palpation of the ACJ then injury there is unlikely
  2. ACJ injury is graded with the Rockwood Classification I-VI
  3. ACJ sprain would show minimal disruption on radiograph and be managed with a sling

References 

(1) Renfree KJ, Wright TW; Anatomy and biomechanics of the acromioclavicular and sternoclavicular joints. Clin Sports Med. 2003;22(2):219.

(2) Montellese P, Dancy T; The acromioclavicular joint; Prim Care. 2004;31(4):857.

(3) Walton J, Mahajan S, Paxinos A, Marshall J, Bryant C, Shnier R, Quinn R, Murrell GA; Diagnostic values of tests for acromioclavicular joint pain; J Bone Joint Surg Am. 2004;86-A(4):807. 

(4) Hegedus EJ, Goode A, Campbell S, Morin A, Tamaddoni M, Moorman CT 3rd, Cook C Physical examination tests of the shoulder: a systematic review with meta-analysis of individual tests; Br J Sports Med. 2008;42(2):80.

 

 

 

 

 

 

 

Palpating for AAA - More than a feeling?

An elderly gentleman presents with severe lower abdominal to groin pain resolved with morphine with the ambulance crew.  On abdominal examination you think you can feel a central pulsatile/expansile mass.  You wonder what to do.

Overview:

Abdominal aortic aneurysm (AAA) is the most common true aneurysm.  A true aneurysm is a full thickness focal dilatation of an artery to >50% its original diameter.  95% of the human population will have an aorta <3.0cm in thickness(1) so if a patient is found to have an aorta >3.0cm in diameter then we can consider it to be aneurysmal.  

Risk factors for AAA include:

● Older age 

● Male gender 

● Cigarette smoking 

● Caucasian race 

● Atherosclerosis 

● Hypertension 

● Family history of AAA 

● Other large artery aneurysms (eg, iliac, femoral, popliteal)

Only 20-30% of patients presenting with a ruptured AAA have a known history of AAA(2,3).  50% of patients with AAA present with the classic triad of severe abdominal pain, hypotension and and a pulsatile mass on abdominal palpation(4).  Abdominal palpation can reliably identify a patient with a AAA >5.5cm. Whilst palpation identifies <50% of patients with asymptomatic AAA(5) it will identify up to 62% of patients with ruptured AAA so it is important to look out for(6).   In a study of 200 patients, the overall sensitivity of abdominal palpation for detecting AAA was 68% and the specificity was 75%(7).  The likelihood of successful palpation of a AAA is proportional to the diameter of the AAA and inversely proportional to the patient's diameter.  Palpation of a AAA has never been known to provoke rupture despite what urban legends regarding OSCEs you may have heard!(6).

In all patients presenting with abdominal pain and haematological instability with a known AAA rupture must be considered and ruled out with imaging.  For patients not known to have a AAA but where rupture is suspected imaging is once again essential.  POCUS (Point of Care Ultrasound) can be used but is dependent on the skill of the practitioner and can be degraded by patient habitus or bowel gas however it is a useful rule out tool.  CT can confirm rupture as well as guide management or identity other pathology but doesn't carries risks of radiation and isn't appropriate for severely unwell patients. 

FullSizeRender-14.jpg

Learning Points:

  1.  The majority of patients presenting to ED with ruptured AAA don't have previous history of AAA
  2. Not all patients with ruptured AAA will have the classic triad of pain, low blood pressure and pulsatile mass
  3. The sensitivity and specificity of palpation of a ruptured AAA is high and so ruptured AAA must be considered in all patients with abdominal pain and known AAA or in patients not known to have AAA but presenting with pain and a pulsatile mass 

References:

(1) Johnston KW, Rutherford RB, Tilson MD, Shah DM, Hollier L, Stanley JC, Suggested standards for reporting on arterial aneurysms. Subcommittee on Reporting Standards for Arterial Aneurysms, Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery and North American Chapter, International Society for Cardiovascular Surgery, J Vasc Surg. 1991;13(3):452.

(2) Akkersdijk GJ, van Bockel JH, Ruptured abdominal aortic aneurysm: initial misdiagnosis and the effect on treatment, Eur J Surg. 1998;164(1):29.

(3) Gloviczki P, Pairolero PC, Mucha P Jr, Farnell MB, Hallett JW Jr, Ilstrup DM, Toomey BJ, Weaver AL, Bower TC, Bourchier RG , Ruptured abdominal aortic aneurysms: repair should not be denied, J Vasc Surg. 1992;15(5):851.

(4) Rinckenbach S, Albertini JN, Thaveau F, Steinmetz E, Camin A, Ohanessian L, Monassier F, Clément C, Brenot R, Camelot G, ChakféN, Kretz JG , Prehospital treatment of infrarenal ruptured abdominal aortic aneurysms: a multicentric analysis, Ann Vasc Surg. 2010;24(3):308.

(5) Lederle FA, Johnson GR, Wilson SE, Littooy FN, Krupski WC, Bandyk D, Acher CW, Chute EP, Hye RJ, Gordon IL, Freischlag J, Averbook AW, Makaroun MS, Yield of repeated screening for abdominal aortic aneurysm after a 4-year interval. Aneurysm Detection and Management Veterans Affairs Cooperative Study Investigators, Arch Intern Med. 2000;160(8):1117.

(6) Azhar B, Patel SR, Holt PJ, Hinchliffe RJ, Thompson MM, Karthikesalingam A, Misdiagnosis of ruptured abdominal aortic aneurysm: systematic review and meta-analysis, J Endovasc Ther. 2014;21(4):568.

(7) Fink HA, Lederle FA, Roth CS, Bowles CA, Nelson DB, Haas MA, The accuracy of physical examination to detect abdominal aortic aneurysm, Arch Intern Med. 2000;160(6):833.

 

 

 

 

 

You've Got Some Ex-Spleening to Do

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A man in his 60s with a background of haemolytic anaemia attends with sudden onset LUQ pain. It's sharp in nature and doesn't radiate.  It's severe.  He otherwise feels well.  There is no history of trauma.  He had an ultrasound scan 5 years ago which showed a slightly enlarged spleen.  On palpation you think you can feel splenomegaly.

What and where is the spleen?

The spleen is a major haemopoeitic organ with roles in immunity and filtering the blood for cells and bacteria.  At any one time about 1/3 of our total platelets will be sequestered in the spleen. Due to this filtration role an enlarged spleen is an important differential in any type of cytopenia.  

The spleen sits in the posterior left upper quadrant of the peritoneal cavity adjacent to the left 9th-11th ribs, stomach, colon and left kidney; it's hilum is related to the tail of pancreas.  

Pictures from Gray's Anatomy.

A normal spleen should not be palpable apart from children, adolescents or very skinny adults.  An enlarged spleen is best felt during deep inspiration as this pushes the spleen down against your hands.  

 

Differentials of splenomegaly(1)

● Liver disease – 33 percent (cirrhosis)

● Hematologic malignancy – 27 percent (lymphoma)

● Infection – 23 percent (AIDS, endocarditis)

● Congestion or inflammation – 8 percent (congestive failure)

● Primary splenic disease – 4 percent (splenic vein thrombosis)

● Other or unknown – 5 percent

What could be causing his pain?

Splenic rupture - in 60% of cases of abdominal trauma the spleen is the only intraperitoneal organ damaged.  Atraumatic splenic rupture is rare but potentially life threatening(2) with 6 major causes identified in the literature(3):

● Neoplasm (eg, leukemia, lymphoma) – 30 percent

● Infection (eg, infectious mononucleosis, CMV, HIV, endocarditis, malaria) – 27 percent

● Inflammatory disease/non-infectious disorders (eg, acute and chronic pancreatitis) – 20 percent

● Drug and treatment related (eg, anticoagulation, G-CSF, thrombolytic therapy, dialysis) – 9 percent

● Mechanical causes (eg, pregnancy-related, congestive splenomegaly) – 7 percent

● Idiopathic (normal spleen) – 7 percent

Splenic infarct - classical presentation is with acute LUQ pain and tenderness; caused when the splenic artery or one or more of its sub-branches becomes occluded either by an embolus, infective or otherwise.  Risk factors include splenomegaly and any pro-thrombotic or pro-embolic state.  

Splenic artery aneurysm - the 3rd most common aneurysm in the abdomen after aortic and iliac artery aneurysm. 

Splenic abscess - uncommon infection caused by seeding from another site such as endocarditis.  Typically presents with persistent fever, LUQ pain with or without splenomegaly. 

Learning Points:

  1.  The spleen is higher up than you might think and at risk of injury if the lower left ribs are involved.  Always suspect in handlebar injuries
  2. The spleen must be palpated for properly or you might miss splenomegaly
  3. Splenomegaly is a major risk factor for splenic pathology; always take a Haematology history and ask about symptoms such as night sweats if you suspect 

References:

(1) O'Reilly RA; Splenomegaly in 2,505 patients at a large university medical center from 1913 to 1995. 1963 to 1995: 449 patients; West J Med. 1998;169(2):88.

(2) Carlin F, Walker AB, Pappachan JM ; Spontaneous splenic rupture in an intravenous drug abuser; Am J Med. 2014 Mar;127(3):e7-8. Epub 2013 Oct 29.

(3) Renzulli P, Hostettler A, Schoepfer AM, Gloor B; Systematic review of atraumatic splenic rupture; Candinas D; Br J Surg. 2009;96(10):1114. 

Cartoons courtesy of the always excellent Amazing Yeti.

Being Head Smart

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You see a 15 year old who attends the Emergency Department with a persistent headache.  They have read an article in a newspaper and since then they're concerned they have a brain tumour.  They ask you what you'd look for in case it was a brain tumour.  You wonder where you'd go to find this information.  You'd like some support and don't know where to look.

The Brain Tumour Charity was formed in 2013.  HeadSmart UK-wide campaign based on research funded by The Brain Tumour Charity at The University of Nottingham.  It has fantastic resources on its website.  The focus is on spotting the red flags of brain tumours and how as clinicians we refer and how urgently.

  • Same day referral from primary care if high risk of brain tumour/life threatening symptoms
  • 2 week referral if lower risk but on differential list

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In the latest Take Aurally podcast we were lucky to have Dr Shaarna Shan from HeadSmart join Jamie and Dr Colin Gilhooley our resident Paediatric SpR to discuss the charity, its formation and the diagnosis and referral process of Paediatric brain tumours.  

Learning Points 

  1. Consider brain tumours in any child with headache, visual disturbance, motor signs and symptoms, growth and endocrine symptoms, increasing head circumference, behavioural change, diabetes insipidus, seizures or altered GCS
  2. Remember symptoms can fluctuate
  3. Ask about pre-disposing conditions - personal or family history of brain tumours, sarcoma, leukaemia or early onset breast cancer; Tuberous sclerosis, Neurofibromatosis or other familial genetic syndromes

Remember to check out the HeadSmart website this catchy tune: 

Return of the MACS

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A middle aged man who is normally fit and well presents following 'indigestion' earlier that day which has settled.  He says his indigestion was a burning pain in the middle of his chest which did not move anywhere.  He blames it on overdoing it the night before with food and alcohol.  He looks and feels well now and only came to the department because his father had a heart attack at a similar age.  His ECG is normal.  His Troponin I is 10,000.  The patient is amazed as he is told he's had a heart attack, "but it didn't feel like a heart attack looks on the TV".

First things first - what is an myocardial infarcation?  We're now on our third universal definition of MI and it's important to note the 5 types of MI:

  1. Unstable plaque rupture or coronary dissection
  2. Supply/demand mismatch - such as arrhythmia or anaemia
  3. Sudden cardiac death that includes signs and symptoms of myocardial ischemia, such as ECG changes, but which produces death before a blood sample can be obtained or when death occurs during the lag period before serum markers appear in the blood
  4. PCI related
  5. CABG related

You'll notice nowhere in the definition of MI or in the types of MI does it mention the character of pain.  If we hear the words 'cardiac chest pain' we will all imagine crushing central chest pain radiating to the left arm with pins and needles.  

This is where the work of Professor Richard Body at the University of Manchester is so interesting.  The Manchester Acute Coronary Syndrome (MACS) Decision Tool was discussed in the ACS Take Aurally podcast.  As part of this work the five most sensitive features of the history for ACS were not the pain itself but if it was associated with:

  1. Diaphoresis
  2. Vomiting
  3. Pain radiating to RIGHT shoulder  
  4. Worsening angina
  5. Hypotension

As I mentioned in the #FYEO blog post on Red Flags I find this work fascinating due to it being paradigm shifting.  Whenever I mention this to students it very often produces a 'mind blown' moment.  This is important.

Learning Points

  1. Chest pain is chest pain.  Whether it's 'indigestion', a 'twinge', an 'ache' it needs to be worked up as chest pain.  I talked about this in my presentation on red flags.
  2. Gastritis and GORD is a not a diagnosis for a junior to make; nor is it an ED diagnosis to make without ruling out more serious causes.  Maybe if the patient is well known to have GORD/Barrett's Oesophagus and gives a compelling history but even then the more serious causes have to be ruled out.
  3. There are five kinds of MI.