E • COMPLICATIONS
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85 days following injury. In the great majority, venous thrombosis in the legs was the
underlying cause of embolism, but in some cases pelvic vein thrombosis was found. The
incidence of pulmonary embolism varied during individual years and in one particular
year it was as high as 253 per cent. This was also confirmed by Watson (1968) in a com
prehensive paper on 431 cases of the Lodge Moor Unit, Sheffield, admitted within the
first week after injury. 1965 was the year with the highest incidence of both venous
thrombosis (25 per cent) and pulmonary embolus (5 per cent) as well as death (9 per
cent). The overall incidence of venous thrombosis amongst the 431 cases was 54 (12-5 per
cent), that of pulmonary embolus 22 (5 per cent) and death 7 (1-5 per cent). Watson also
confirmed the highest incidence in complete thoracic lesions, and as in our and Phillip's
cases the left leg was involved twice as often as the right in venous thrombosis. In
accordance with our own observations the highest incidence of venous thrombosis and
embolism occurred within the first 2 months and pulmonary embolism may occur
without previous warning symptoms. There is general agreement of various workers in
this field that thrombosis and pulmonary embolism is much less common in later stages
of paraplegia.
Premonitory signs
The most significant sign of deep venous thrombosis is swelling of the leg, not infre
quently combined with low grade temperature. However, in paraplegics this swelling of
the leg may be obscured by postural oedema, and the low grade temperature may be
mistaken as being caused by active urinary infection. The diagnosis of deep venous
thrombosis can be made if by changing the position of the patient the swelling does not
soon disappear whether or not raised temperature is present.
However in pulomonary embolism any premonitory sign may be completely absent
and the following case is a typical example. It is described in detail as the patient recovered
and showed most interesting symptoms during recovery:
C.H., aged 43, was admitted to Stoke Mandeville on 6 August 1958 with a complete
tetraplegia below Cy/8 following fracture-dislocation below C6/y sustained on 2 August
1958. He was treated with skull traction and intermittent catheterization and the urine
was kept sterile. On 14 September 1958 (43 days after injury) at 9.50 a.m., when treated
by a physiotherapist moving his left leg, he suddenly felt 'queer5 , grew pale and became
unconscious. He was seen i minute later by Dr Michaelis who found him unconscious
with eyes widely opened, slight rotatory nystagmus, pulse very weak and irregular,
Cheyne-Stokes breathing, upper chest cyanotic. When I saw the patient 10 minutes
later (10 a.m.) he was pulseless, no nystagmus, corneal reflexes absent, respiration stopped.
Oxygen and artificial respiration had been started almost immediately and coramin
injections were given intravenously and intramuscular.
At 1010: Slow return of colour and irregular pulse. Still deeply unconscious.
1015:
Pulse 80, regular, B.P. 130/45, respiration improving, unconsciousness less
deep, corneal reflexes weakly positive.
1030:
Responding to calling his name, moaning. Oxygen and artificial respiration
continued.
