This post is based on the talk Andrew Tagg was invited to give at BadEMFest20 in Capetown. Unfortunately, world events made that a little challenging.
Humans evolved from Homo erectus to Homo sapiens around 500,000 years ago. Fossils dug up from by the Leakeys in Olduvai Gorge, Tanzania, revealed how we moved from shuffling knucklewalkers to the upright hominids we recognize today. Walking on two legs allowed us the freedom to use our hands – to communicate, to use tools, and to keep ourselves safe.
How do we walk?
The normal human gait is comprised of three distinct phases:
- The contact phase – from heel strike to flat foot
- The stance phase – from flat foot to heel off the ground
- The swing phase – the propulsion phase as weight transfers from the toes
The swing phase normally comprises 40% of the gait cycle.
Like Sherlock Holmes or his progenitor, Joseph Bell, if you watch your patient walk you can get a lot of clues as to the potential underlying pathology before you even exchange a word with them or their parents.
This hobbling gait has a normal contact phase and normal propulsion with a decreased stance phase. In essence, the patient is trying to decrease the amount of time spent bearing weight through the hip joint itself.
In this gait disturbance, the hip muscles are too weak and so the unaffected side drops towards the floor. It suggests a biomechanical issue such as ass avascular necrosis, or a slipped capital femoral epiphysis.
The patient swings their leg out and around to clear the floor. This is often due to a leg-length discrepancy in the delayed diagnosis of developmental dysplasia of the hip (DDH).
Toe walking, though normal up to the age of three may suggest that the child is unwilling or uncomfortable engaging their gastrocnemius muscles in walking. This can occur in many conditions.
The rate of presentation to the emergency department with an atraumatic limp is approximately 1.4 per 1000 in children under the age of 14. It occurs more often in boys than in girls (1.7:1) and the median age is 4.4 years. When we consider the potential causes the list is massive. In this post, we are going to concentrate on both the more common conditions and those diagnoses that we really shouldn’t miss. Whilst any part of the limb might be the cause (from the toes to the hip) this post is going to focus on causes centred around the hip joint. They account for about 60% of cases of limp. That doesn’t mean you shouldn’t look in their shoes for pebbles or look at their toes though!
Let’s break it down to some age-specific diagnoses and those that can occur at any age
Late presentation of developmental dysplasia of the hip (DDH)
It is just possible that routine screening with Ortolani’s and Barlows test might have missed a case of hip dysplasia. The limb resultant limb shortening can be hard to detect if it is bilateral but this is one time to get out the tape measure and look for a leg length discrepancy as you measure from anterior superior iliac spine (ASIS) to medial malleolus.
If you don’t have a tape measure to hand then look for a positive Galeazzi sign, suggesting a shorter hip segment on the affected side.
This diagnosis accounts for the majority of cases of atraumatic limp and may follow an upper respiratory tract infection though the evidence for causation is poor. It is most common in young boys, aged 4 to 8 years of age and is self-limiting in nature. It’s a diagnosis of exclusion rather than anything else made easier by the well-appearing, afebrile child. It should respond to simple NSAIDs though is recurrent in 20% of cases.
According to Viera and Levy, bedside sonography has a sensitivity of 90% and specificity of 100% to detect an effusion. Unfortunately, it doesn’t help with determining the cause.
It’s beyond the scope of this post to talk about NAI and long bone injuries in children (especially as Nikki Abela did such a great job at DFTB18) so instead, it’s worth thinking about toddlers’ fractures. These occur due to torsional force on the tibia, accompanied by a fall, and may only be picked up as tenderness over the distal third of the tibia. That first set of x-rays performed in the emergency room may not show any obvious pathology with signs only becoming obvious after a couple of weeks. This is one of those occasions where ultrasound may be much more helpful though if clinical suspicion remains it should be treated with immobilization and close follow-up. Repeat imaging may then show the beginnings of some callus formation or a radionuclide bone scan may be needed. If they are not toddling and waddling it is not going to be a toddler’s fracture.
Although unlikely to present as an isolated limp, cerebrovascular events may present as hemiparesis; It’s beyond the scope of this post to go into them in more detail. Watch this space.
This is idiopathic avascular necrosis of the growing femoral head and typically presents in boys at the younger end of the scale (4 to 8 years old). Because of this, these children are often shorter than their peers and there is a possible association with hyperactivity. The classical findings on a plain AP x-ray of the pelvis include sclerosis leading to destruction and the eventual collapse and flattening of the femoral head. As this is a biomechanical problem, they might present with a slow onset antalgic gait with pain on internal rotation and ABduction. Around 20% of cases are bilateral.
Both MRI and bone scan are equally sensitive if the plain films are equivocal. Treatment may be surgical or conservative depending on the degree of bone destruction and the age of the child. Left unchecked neovascularization occurs with the destruction of the femoral head.
Though first described in 1897, it was not until 1910 that it was found to be unrelated to tuberculosis. Arthur Legg, Jacques Calvé and Georg Perthes are guilty of its eponymous name.
I think we’ve said enough about transient synovitis already.
As well as a stroke a limp might be the initial feature of an ascending paralysis in Guillain-Barré. We’ll talk about that and ADEM another time.
Slipped Capital Femoral Epiphysis
A slipped capital femoral epiphysis or slipped upper femoral epiphysis is more common on older, overweight boys, over the age of 10 years of age. There is often a structural weakness of the physis itself so it is more common in cases of endocrine dysregulation (such as hypothyroidism) and metabolic conditions (such as renal osteodystrophy). The proximal epiphysis displaces anteriorly and laterally relative the metaphysis. Involvement of the medial obturator nerve may mean that they present as knee pain rather than hip pain. Early fixation and we mean in less than 24 hours in unstable cases, can ward off the threat of life-long pain and deformity. Plain AP films may not be enough in the case of subtle slippage. So if you are suspicious then you should go ahead and order a lateral film as well. A lot of other hip pathology is made easier to spot in a frog-leg lateral. Don’t do this if you are suspicious of a SCFE, you might make things much, much worse.
Look for Klein’s line. A line along the superior aspect of the femoral neck should intercept with the epiphysis. Imagine it as an ice cream slipping off the cone on a hot summer day.
Some things need to be in our differential no matter the age of the child.
The hip is the most commonly infected joint with the haemategenous spread of organisms grown dependent on the local flora. Young children (under the age of 2), those who are immunosuppressed or asplenic are at higher risk. In Australia, for instance, the commonest organisms grown are Staphylococcus aureus and Group B Streptococcus (especially now that Haemophilus influenzae b infections have been almost wiped out by immunization). In the youngest, patients consider the weirder organisms like Kingella kingae and Salmonella (in patients with sickle cell disease).
The juvenile physis does not prevent the spread from a remote source from entering the epiphysis and so haematogenous spread (rather than direct local invasion) is often the culprit. The hip is classically held in a position of external rotation, ABduction and, flexion, perhaps in an effort to maximize the joint space and minimize the pain.
It would be great if there was a way we could differentiate the serious diagnosis of septic arthritis from something less serious, such as transient synovitis. Step forward Meninder Kocher et al. and their seminal paper.
Kocher MS, Zurakowski D, Kasser JR. Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm. JBJS. 1999 Dec 1;81(12):1662-70.
They looked at 17 years of data for patients that presented to a single tertiary hospital with an acutely irritable hip. This amounted to 282 cases in all of which only 168 had their hip joint aspirated. Of this 168, only 26 had true septic arthritis as confirmed by a positive culture of joint aspirate or 50,000 WCC in the aspirate with a positive culture, 9 had a positive joint culture and negative blood cultures and 3 had only positive blood cultures. By performing a multivariate analysis they then looked for key indicators that differentiated cases of septic arthritis from the more benign irritable hip. Four key factors cropped up. They were a history of fever, inability to bear weight, a WBC greater than 12 x 109/l and an ESR ≥ 40mm/hr. If you had none of these then the probability of having septic arthritis is 0.1%. But if you have all four it jumps to 99.8%.
Of course, this is all the primary literature that most people read but when Kocher tried to validate the study having all four markers gave the chance of having septic arthritis as 93% and when Luhmann et al. tried to externally validate the criteria it dropped to 59%. Caird et al. must have realized that not many of us use ESR any more and so appended the more common C-reactive protein (CRP). Having all 5 gave a 97.5% positive predictive value though there were only 14 cases of transient synovitis, and 5 of septic arthritis.
An indolent course and a non-specific physical examination make this a difficult diagnosis to pick up at first glance. Around 1.5-2% of all children presenting with an atraumatic limp will have osteomyelitis. Plain films may be unremarkable early in the course of the illness and only show periosteal changes after a week to 10 days. An MRI scan is more sensitive and if the diagnosis is still a challenge then radionuclide scanning might pinpoint the infection. The hip is one of the more common joints affected (25%) followed by the tibia/fibula (25%) then the humerus (13%). Osteomyelitis and septic arthritis can coexist as infection from the bone spreads to the joint capsule.
One case series suggests that 40% of cases are due to transient synovitis, chronic muscle sprain or trauma accounted for 16% and no diagnosis was made in 30%. All those diagnoses we have to learn for exams are much less common (Perthes’ disease 2%, osteomyelitis 1.5%, toddlers’ fractures 1%, and SCFE 1%). What has not been mentioned, as the incidence is incredibly low is the thing that many parents worry about – cancer.
Whilst parents may not have heard of a slipped capital femoral epiphysis or Kocher’s criteria but they have heard of cancer and so we need to address it. Primary benign tumours (unicameral bone cysts, for example, as well as malignant ones can present as bony hip pain. Hip pain can also be a presenting feature in haematological malignancies such as acute lymphoblastic leukaemia. The most common malignant bone tumours in infants are osteogenic sarcoma and Ewing’s sarcoma. Both of these are most common in the second decade of life.
Persistent pain, coupled with constitutional symptoms such as night sweats, weight loss and night pain are highly suspicious and should prompt imaging and blood tests.
Please, Just STOP LIMPING from Tim Horeczko and the PEM Playbook
Septic arthritis from PEM Morsels
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