Chapter 31 Back pain in the elderly
Case 31.1
Possible diagnosis | Justification |
---|---|
Central spinal stenosis | |
Circulatory problems | |
Neuralgia due to inflammation/infection/tumour(s) | |
Polymyalgia rheumatica |
To differentiate between mechanical, infectious or circulatory origin of the symptoms.
Case 31.2
Possible diagnosis | Justification |
---|---|
DDx 1: abdominal aortic aneurysm (AAA) | Patient’s age, sex, history of smoking, sedentary lifestyle, severity of pain, pale complexion and history of hypertension would indicate a rupture of an AAA. Because the pain had been present in the week preceding presentation and because the patient has not lost consciousness, despite displaying the signs of hypovolaemic shock, it is possible that this is a leak, rather than a rupture |
DDx 2: lumbar compression fracture secondary to bony metastases from prostate cancer | Low back pain may be due to metastatic lesions in the lumbar spine resulting in a pathological fracture. This is based on the severity of pain, history of urinary problems, mode on onset and pain not relieved by painkillers |
DDx 3: mechanical pain of musculoskeletal origin | Mode of onset, age, previous history of low back pain, achy pain developing to sharp pain as in acute facet sprain |
DDx 4: abdominal pathology (eg: appendicitis or gastrointestinal inflammation) | Right groin pain may be from appendicitis, pale complexion may be from systemic condition and low back pain may be referred from gastrointestinal tract |
DDx 5: a combination of 3 and 4 |
Pain which is aggravated by movement suggests that the problem is within the musculoskeletal system.
With hypotension, increased sympathetic tone causes tachycardia (>100 bpm). During hypovolaemic shock, although the blood pressure may be maintained initially, hypotension develops from loss of circulating blood volume (systolic <100 mm/hg).[1]
David needs immediate emergency referral to the local hospital’s accident and emergency department. An ambulance should be called and David should not be moved until the paramedics arrive to minimise the risk of further rupture and haemorrhage. Rupture of an AAA is responsible for 5800 deaths in men and 3500 deaths in women per year in the UK[2] and 0.8% of all deaths per year in the USA.[3] The mortality rate of AAA rupture is reported to be between 78% and 94% in the USA compared to less than 5% for elective surgical repair of an asymptomatic lesion.[3]
Initial screening of a suspected AAA is done by the use of abdominal ultrasound. Although it is recognised that computed tomography (CT) scanning is the definitive means of assessing the size of AAA,[4] some studies suggest that ultrasound gives a more accurate determination of true maximal AAA diameter.[4] Scanning is required to assess the size of the aneurysm and also to asses for rupture and blood leaking into the abdominal cavity or retroperitoneal space. In David’s case you would expect to see an enlarged section of aorta, consistent with an aneurysm, and based on the history of abdominal pain and signs of hypovolaemic shock, rupture of the vessel wall.
There is some debate in the literature as to what risk factors are specific to the cause of AAAs and at the moment it is possible to say that the exact cause is unknown. It would appear that older age (over 60 years), male gender, smoking and family history of AAA all contribute to an increased risk of developing AAAs.[3,5,6,7,8] Traditionally, hypercholesterolemia was thought to play a role in the development of AAA through the process of atherosclerosis. Although AAA is not a direct result of atherosclerosis, atherosclerosis does appear to contribute to AAA development.[8] Interestingly, diabetes appears to have a protective effect against AAA formation. Hypertension, although not a risk factor for the development of AAAs, appears to increase the growth rate of already established AAAs.[8] Genetic diseases, such as Marfan’s and Ehlers-Danlos syndrome, also increase the risk of developing AAAs.