Saturday 26 April 2008

Ethics in Medicine

Dear Bloggers

I sometimes like to do an article based on ethics. Medicine is not just about trying to make a diagnosis and treating everything that is a problem. Medicine is not just a science project that can be controlled like a laboratory experiment. Medicine is a mix of science, personal interactions, subjective and objective opinions from the doctor, the patient and the family with the abundance of feelings all intermingled.

Ethics is a very important part of medicine and is used perhaps unknowingly all the time when making decisions on how to proceed with patient care.

I have observed that the ethical dilemmas are different in Japan compared to the UK. For example, sometimes patients in Japan do not have the finances to be able to pay for expensive treatments and so on occasion, families will make the decision for the patient which may sometimes lead to an alteration of therapy which may not be what the medical staff would advise or think is appropriate. In the UK, taxation pays completely for the medical system and use of medical services is free at source, and hence, treatments are started if there is a clinical need and the patients and their families do not consider the financial aspects as is done in Japan. However, in the UK, I have said that treatments may be started if there is a clinical need. This is where ethics comes into play because although certain treatments are available, all patients are different, and just because certain investigations and treatments can be done it does not necessarily mean that it is appropriate to do such things either because of the patient's refusal or because of severity of illness, reduced life expectancy, poor quality of life etc...

There is often the saying here of 'All or Nothing' treatment. Either you do everything for the patient or do nothing. I have to say that I really do not agree with such a concept to apply to every patient scenario. Life is not always so black and white-- in fact, life is different shades of grey.

For example, should an elderly patient with a pre-morbid history of severe debilitating chronic disease with profound sepsis and fulminant multiorgan failure with a poor quality of life receive expensive extra-corporeal Polymixin therapy, haemodialysis and receive cardiopulmonary resuscitation when such interventions are very unlikely to cause the patient to survive and moreover, would be unlikely to alter the underlying pathology and importantly, cause more unneccessary discomfort?

There are doctors who might say yes. There would be many who would however say no. This is where ethics comes into the situation. Not everything is so clear cut.

Although haemodialysis removes the toxins from the blood, in the presence of DIC, the use of heparin during dialysis in the treatment of renal failure can worsen bleeding! Haemodialysis is a renal replacement intervention but it does not make the kidneys recover any better! It is purely supportive whilst waiting for the kidney to hopefully recover. However, fulminant renal failure might not recover leaving a patient with an additional chronic diseases and worsening quality of life left on thrice weekly haemodialysis which the patient and their family might not be able to afford. Such therapy might prolong life but might be seen by the patient as inhumane and intolerable. From my observations over the years, doctors frequently forget to consider the end outcome when starting major intervential therapies such as haemodialysis or intubation with ventilation therapy in such patients e.g. terminal lung cancer with respiratory failure.

The great anf famous textbooks show us how to think about symptoms and signs of disease, how to investigate and treat but never about the ethical issues and appropriateness of treatment. For this, the only real textbook is experiencing these situations yourself in the hustle and bustle of daily hospital life. Yes, there are many ethics books available with excellent examples of dealing with difficult issues and I would highly recommend reading such books.

Continuing on, patients with severe sepsis have a very high mortality [over 50% ] in various studies despite optimal treatment. Hence, in such a severe situation, even if there is eventual cardiopulmonary arrest, is it appropriate to perform cardiopulmonary resuscitation? One has to think about the overall outcome. If cardiopulmonary resus is successful, will that stop it from happening again? Will it make the other organs recover? The answer is usually no. One has to consider factors such as cerebral damage of CPR, the potential chronic heart disease resulting from ischaemia of the cardiac arrest, the likelihood of success and I come back to the point once again of Quality of Life.

Many patients with severe chronic disease have a shortened life expectancy and poor quality of life. In the UK, patients are asked directly about whether they would want to be resuscitated rather than asking the family. The family memebers are not the patient and in the UK, they are regarded as separate entities and therefore are not able to make such life and death decisions about the patient unless the patient is a child. On occasion, UK patients will directly state that they do not want to be resuscitated despite the contrary opinion from their relatives. Obviously, if the patient is not confused and not suffering from a psychiatric illness, and is considering such an opinion in a logical, clear way, the doctors have to respect the decision of the patient over that of the relatives. The patient is put first.

However, in Japan, the wishes of the family sometimes over-ride the wishes of the patient and sometimes, the patient is not directly consulted. There is the fear of family members that such discussions might make the patient's mental condition worse and that they will somehow 'die from shock' or that the patient would somehow not want to know their fate. From my experience of direct talking to patients in the UK, I have never experienced such spontaneous death from a discussion about the patient's condition directly with the patient and hence, such thoughts are somewhat unfounded in my opinion. Moreover, doctors siding with family members to avoid informing the patient of the diagnosis is again unfounded. As I have mentioned in a previous blog dealing with ethics, by informing the patient allows family members to be entirely honest with eachother in the final days, weeks or months of terminal illness which has the benefit of bringing family members closer together.

Hence, when we are considering whether to institute a treatment, we need to consider not only the medical problem in front of our eyes, but also the social factors and particularly Quality of Life issues. Doing knee-jerk reactional therapy with the 'Do All Or Nothing' approach is ignoring the Ethical issues which might be in direct conflict of the wishes and the interests of the patient.

Another concern I have about family oriented decisions rather than patient oriented decisions is when family members have a potential vested financial interest to gain from the patient's death. Hence, it is my belief that medical personel should be making the decisions when it comes down to investigating and treating the patient albeit still taking into account the opinion and feelings of the family. However, medical personel can look at the patient and their problems in an independent, unfettered manner to decide just what therapies are appropriate. In doing so, it removes a serious conflict of interest that might potentially exist between the patient and the family members interests.

Palliative care is another area which needs much development in Japan and it is entrenched with ethical issues. I have written on Palliative Care in the past and I see this as a very important arm of medicine. Patients should not be put through pointless operations for cancer that have no hope for prolonging life when the other intervention would be controlling pain and other symptoms to make life as happy and tolerable as possible during the final stages of illness. Using a palliative approach is Not a Failure of the Doctors! Sometimes, diseases can no longer be controlled by 'modern' medicine and pursuing treatments which do not alter the final outcome and cause more pain and suffering is not putting the patients first. Although as medical people it makes us feel better that we have tried our best and shows the family that we are really trying to do everything, the patient can get lost in the mix and it might not be the best for them!

One has to ask what is best? Doing everything to make us and the family feel better at the expense of the patient's feeling both mentally and physically or putting the patient first and using ethics based ideology to decide on whether the patient really wants such treatment and whether it will lead to a favourable outcome. Hence, palliative care is sometimes better than 'full active' treatment as pain, agitation, dyspnoea etc can be controlled through symptomatic measures and medications.

When I started off in medicine I thought that medicine was just about saving people from dying of illnesses. Yes, that principle I still hold true and is the driving force for my love of medicine. However, I learned over the years, that not all patients can be saved from the natural course of their illness and having a humane passage out of this world by using appropriate palliative interventions rather than futile active treatment, is sometimes better than doing everything and still losing the battle with the patient suffering more as a result.

Please remember about ethical issues and think about your patient as a whole being, rather than just a system disease based approach. Please consider....

Have a nice day....

Wednesday 23 April 2008

Answer To Recent Case- Acute Weakness and Sensory Impairment

Dear Bloggers

Here is the answer to the recent case.


Question 1: From history and examination, list the problems with this patient

  • Rapidly progressive weakness of the lower limbs with numbness
  • Ascending sensory level to T10
  • Bowel and bladder disturbance
  • Loss of muscle power, deep tendon reflexes and Babinski absent in lower limbs
  • Incomplete presence of light touch and vibratory sense; absent nociception and thermoreception
  • Loss of anal tone and 'wink' sign
  • Hypertension
  • Smoker
  • Mildly expansile aorta
Question 2: What immediate test or tests would you perform and why?

From the acute history of weakness and numbness progressing over minutes, loss of bowel and bladder function with progression over several more hours is consistent with a acute spinal cord condition either from external compression or impairment of blood supply or a transverse myelitis.
The patient was otherwise well and was afebrile on admission, making a viral infection less likely. Moreover, there was no history of previous back problems e.g. disc herniation. The fact that the patient is a smoker and hypertension are cardiovascular risk factors and with this history, it is consistent with an acute spinal cord infarction.

The immediate test would be do perform an MRI to rule in or out a spinal cord compression. An abdominal ultrasound or CT to look for an aortic aneurysm would also be prudent if there was a history of abdominal pain and/or an abdominal aorta consistent with aneurysmal change. An ECG should be performed to look for atrial fibrillation which might contribute to systemic embolisation. Echocardiogram would also be worthwhile to rule out a cardiac source of embolism e.g. intra-atrial thrombus, vegetation from endocarditis.

Question 3: What anatomical problem is this from the history and physical examination?

The anatomical problem is two-fold. Firstly, the blood supply to the spinal cord has been impaired and this has led to infarction. However, from the physical examination, the nociception and thermoreception plus motor are predominantly impaired whereas a modicum of light touch and vibratory sense are maintained.

In view that the anterolateral cord contains the descending long tracts (corticospinal tracts) and the ascending spinothalamic tracts (pain and temperature), it would appear that the anterolateral cord is most affected with less of the dorsal cord affected which convey senses such as light touch and vibratory sense. However, strangely, the joint position sense was impaired which also runs up the dorsal columns. This cannot be easily explained unless the patient already had an existing peripheral neuropathy prior to the onset of this disorder e.g. diabetes mellitus.

In view that there is a single anterior spinal artery supplying the anterior cord and two posterior spinal arteries, this problem is consistent with an anterior spinal artery occlusion and anterolateral cord infarction.

Question 4: What is the current evidence based treatment for such a condition?

There have been many proposed therapies including anti-platelet treatment, anti-coagulation, thrombolytic therapy. This condition is relatively rare and so being able to perform a randomised control trial is difficult. Hence, most treatments are based on a case by case basis.
However, therapy is similar to that of cerebral infarction.

To date, there has been only one published case of using thrombolysis in a patient with this problem, although I have heard of another case of spinal cord infarction where thrombolysis was also used [unpublished] with good results.


Tex Heart Inst J. 2007;34(1):134-5.

Acute spinal cord ischemia during aortography treated with intravenous thrombolytic therapy.
Restrepo L, Guttin JF.

In the above case, the infarction occurred after aortography rather than de novo without an inciting cause.

In this case, anti-platelet therapy was commenced without modification of the patient symptoms and following this, heparin was commenced. The patient did not receive rTPA.

There was a minimal response to therapy with only a slight improvement in sensation but no improvement in motor response. It is therefore not certain whether the mild improvement was related to the treatment or just the natural course of the condition.

The intial MRI scan showed some osteoarthritis high up in the neck but not considered to be the cause of the symptoms when reviewed by the neurosurgeons. The cord proper looked normal.
A repeat MRI taken after several days again looked normal.

CSF examination was not performed.

ECG showed sinus rhythm and the echocardiogram revealed no thrombus. Abdominal echo revealed no evidence of an abdominal aortic aneurysm.

Arteritis was also considered but the ESR was within the normal range for age and sex.

Several doctors have kindly responded to the case and include Professor Alan Lefor, Professor of Surgery, Jichi medical school, Japan gives a surgeons view of the history and physical followed by the kind Dr Masami Matsumura of Kanazawa University School of Medicine with an indepth and excellent break down of the case into its essential elements. Thanks to both these esteemed doctors for their opinions here.

Professor Alan Lefor:

To me, a case of acute paralysis and anal sphincter loss of tone, is an acute spinal cord problem such as trauma (no history here), spinal cord ischemia (like a dissection, but in the absence of pain might not be as high on the list, although she does have hypertension) or spinal cord compression (like a tumor, hematoma).

My workup would start with a CT scan to evaluate the aorta and spinal canal looking for dissection, aneurysm, and spinal canal mass.

Rx for a dissection would be htn control.

Dr Masami Matsumura:

Questions
1) From history and examination, list the problems with this patient.

Problem list:
#1 Numbness of the buttocks
#2 Rapid onset lower limb weakness, then paralysis of the lower limbs
#3 Reduced muscle tone
#4 Reflexes knee (L2-4) absent, ankle (S1) absent
#5 Light touch- decreased in lower limbs up to the umbilicus (Th10) region
#6 Vibratory sense (posterior column) was intact on the pelvic brim (S3) and right knee (L4) but absent further down
#7 Nociception and thermoreception were absent.
#8 Reduced anal tone (S2-4)
#9 Bowel and bladder disturbance.
#10 Absence of joint position sense (posterior column)
#11 Hypertension
#12 Smoking history
#13 Aorta mildly expansile

Assessment:
At the beginning, this patient is 70 years old woman who has history of HTN and smoking. I would use following system for thinking differential diagnosis in view of weakness. I would differentiate neoplastic or degenerative diseases first.

Vascular: possible, infarction of spinal cord, arterio-venous malformation
Infection: less likely,spinal epidural abscess,Lyme disease, syphilis
Neoplastic: possible, vertebral or spinal cord tumor, metastasis ofbreast cancer, lung cancer,gastrointestinal cancers,or renal cell carcinoma, non-Hodgkin's lymphoma, plasmacytoma, multiple myeloma, orparaneoplastic syndrome
Collagen: possible, sarcoidosis, polymyositis, vasculitis, Guillan-Barre syndrome, SLE (very rare)
Toxic/Metabolic: less likely, periodic paralysis, hypokalemia
Trauma/Degenerative: possible,intervertebral disk disease or spinal stenosis,
Congenital: less likely
Iatrogenic: less likely
Idiopathic: less likely,amyloidosis

Cauda equina syndrome is likely in this case from problem #1 to #10.
#1 Numbness of the buttocks
#2 Rapid onset lower limb weakness, then paralysis of the lower limbs
#3 Reduced muscle tone
#4 Reflexes knee (L2-4) absent, ankle (S1) absent
#5 Light touch- decreased in lower limbs up to the umbilicus (Th10) region
#6 Vibratory sense was intact on the pelvic brim (S3) and right knee (L4) but absent further down
#7 Nociception and thermoreception were absent.
#8 Reduced anal tone (S2-4)
#9 Bowel and bladder disturbance
#10 Absence of joint position sense (posterior column)

Cauda equina syndrome is included in concept of epidural spinal cord compression (ESCC).

UpToDate 16.1 describes as follows:
Neopalastic ESCC is a common complication of cancer that causes pain and sometimes irreversible loss of neurologic function. In adults, the tip of the spinal cord usually lies at the L1 vertebral level; below this level, the lumbosacral nerve roots form the cauda equina, which floats in cerebrospinal fluid. With cauda equina lesions, the weakness is associated with depressed deep tendon reflexes in the legs.

My first question is as follows:
Can we interpret problem #5 Light touch- decreased in lower limbs up to the umbilicus (Th10) region as a finding of cauda equina syndrome?
UpToDate 16.1 describes as follows:
When a spinal sensory level is present, it is typically one to five levels below the actual level of cord compression. Saddle sensory loss is commonly present in cauda equina lesions, while lesions above the cauda equina frequently result in sparing of sacral dermatomes to pinprick.

Cauda equina syndrome can cause decreased light touch in lower limbs up to the umbilicus (Th10) region.

My second question is as follows:
Why she doesn't have back pain?

UpToDate 16.1 describes as follows:
Pain is usually the first symptom of ESCC, being present in 83 to 95 percent of patients at the time of diagnosis.
This patient didn’t complain back pain. But 5 to 17 percent of ESCC cases don’t disclose back pain.

Third my question is as follows:
What is the cause of her cauda equina syndrome?

UpToDate 16.1 describes as follows:
The three most common are prostate cancer, breast cancer, and lung cancer, each of which accounts for about 20 percent of cases.

This patient is woman and smoker.Vertebral or spinal cord tumor, metastasis of breast cancer, lung cancer, gastrointestinal cancers, or renal cell carcinoma, non-Hodgkin's lymphoma, plasmacytoma, or multiple myeloma must be differentiated.

Problem #13 Aorta mildly expansile is probably caused by #11 Hypertension.

Questions
2) What immediate test or tests would you perform and why?
MR imaging

UpToDate 16.1 describes as follows:
MR imaging offers several potential advantages over myelography.
It produces anatomically faithful images of the spinal cord and intramedullary pathology and is even more sensitive than radionuclide bone scans at identifying bony metastases. It can image the entire thecal sac regardless of whether a spinal subarachnoid block is present. It is not contraindicated with large brain metastases, thrombocytopenia, or coagulopathy. It spares the patient a lumbar puncture.

Questions
3) What anatomical problem is this from the history and physical examination?
From the history and physical examination, cauda equina syndrome is likely. Neoplastic disease or degenerative disease including spinal canal stenosis might be the cause of L1 or L2 vertebral level compression.

Questions
4) What is the current evidence based treatment for such a condition?
Administration of corticosteroids is first strategy. Next surgical management with anterior decompression should be considered. If diagnosis is neplastic, radiotherapy or chemotherapy should be planned.

UpToDate 16.1 describes as follows:
Management include the administration ofcorticosteroids(dexamethasone ), followed either by surgery and/or radiotherapy (RT). Aggressive surgical management with anterior decompression appears to give better results than RT alone in patients who are candidates for surgical intervention. Compared to RT alone, surgery followed by RT is associated with better neurologic outcomes. Chemotherapy may be beneficial in patients with chemosensitive tumors.

Interestingly, both Dr Matsumura and Professor Lefor listed spinal cord ischaemia / infarction as part of their differential diagnoses from the history and physical examinations. This is the most important thing.

The case by itself without the advanced imaging studies is very difficult to make an accurate diagnosis and in this case, MRI did not show an obvious mass lesion or even the usual cord infarction pattern. However, with the history of rapid onset, paralysis and sensory loss affecting specific sensory modalities, and a non-diagnostic MRI scan, spinal cord infarction was still considered the most likely.

This was later confirmed by a most excellent neurologist.

Summary

In summary, spinal cord ischaemia is rare accounting for <1% of all strokes. Most spinal cord ishaemia occurs due to abdominal surgery. The spinal cord is supplied by one anterior spinal artery and two posterior spinal arteries. Superiorly the vessels originate from the vertebral arteries and they receive feeding radicular arteries from many levels with many coming from the intercostal arteries.
The Adamkiewicz artery is most commonly affected. Studies have shown that the most probable cause of infarcts is related to mechanical stress affecting the radicular arteries which can extend for several levels. Vertebral body infarcts can also occur and are associated with cord infarction and can be another sign of radicular artery occlusion.

There is an association of spinal cord ischaemia and spinal disease and in such chronic compressive diseases there is impairment of blood flow which can impair collateral blood supplies putting at risk the compensatory mechanisms in the event of ischaemia.

Transient ischaemic attacks affecting the spinal cord can also occur.

Clinical Features Associated with Various Types of Spinal Cord Ischaemia

Anterior spinal artery territory- bilateral motor impairment with spinothalamic impairment

Posterior Spinal artery territory- bilateral motor impairment with dorsal column sensory impairment

Complete [transverse] infarct- Bilateral motor impairment with total sensory loss at and below the area of the ischaemia.

Unilateral infarcts produce a hemiparesis, in the case of anterior impairment, a contralateral spinothalamic deficit and with a posterior impairment, a unilateral dorsal column impairment.

[please review the neuroanatomy of the various sensory pathways-- spinothalamic neurones cross over at the level of entry and traverse to the contralateral side and ascend in the lateral spinothalamic tracts whereas the dorsal column input ascends directly from the site of entry and cross over in the brainstem region. The routes of these two pathways explain why there is a difference in the sensory impairment within the spinal cord and different findings on physical examination].

There are no clear guidelines for treatment as there have been no prospective clinical studies and various anti-thrombotic / anti-coagulation measures have been tried in previous cases. In my opinion, a prospective study seems unlikely to be able provide a clear answer because of the paucity of such strokes.