11. Discussion
What to write
Discussion (including conclusion):
11a – Strengths and limitations of the management of this case
11b – Relevant medical literature
11c – Rationale for conclusions (including assessment of cause and effect)
11d – Main “take-away” lessons of this case report
Explanation
Case reports may offer new perspectives on new or rare diseases, unusual disease presentations, therapeutic interventions, or harms1. Succinctly discuss the key features of the case and what was learned. Basic mechanisms or principles (e.g., pathophysiological, immunological, social) and diagnostic challenges may be important, particularly if they help explain observations. Compare the results in the case with results from clinical trials and case reports2,3. Support recommendations for additional research with published references. It is important to transparently discuss limitations, including mentioning that the results from a single case may not be applicable to patients in general2.
The conclusion section is often brief and focuses on the primary lessons learned from the case report.
Examples
11a—Strengths and limitations of the management of this case
“The data which we have presented here have been limited by the restrictions of clinical practice, and in the appendix, we have outlined the major shortcomings of the pharmacokinetic calculations we have made. However, despite the difficulties in deriving accurate estimates of the true apparent volumes of distribution involved, the changes we have observed are too large merely to be accounted for by pharmacokinetic inaccuracies; indeed, any overestimation of the true volumes strengthens the argument. We believe that the changes we have observed are real and have contributed to the digoxin toxicity which occurred in these patients. Further characterization of the cause of the abnormal distribution of digoxin in renal failure by more precise prospective clinical studies is required.”
From Altered distribution of digoxin in renal failure—a case of digoxin toxicity?4
11b—Relevant medical literature
“Dr Barnard successfully used a hypothermic perfusion system to protect a donor heart for more than 16 hours in heterotopic HTx5. However, surgeons are more conservative while performing orthotopic HTx. Few series are using donor hearts with IT longer than 6 hours. Long-term follow-up of HTx recipients at Columbia University in New York and Alfred Hospital in Australia has demonstrated that prolonged IT (average 5 hours) did not adversely affect immediate or long-term survival or the incidence of transplant coronary artery disease6,7. The University of Western Ontario in Canada and The University of Alabama at Birmingham have also demonstrated that long-term survival of HTx was not affected by prolonged IT (longest times 457 minutes and 479 minutes, respectively)8,9.”
From Successful heart transplantation after 13 hours of donor heart ischemia with the use of HTK solution: a case report10.
11c—Rationale for conclusions (including assessment of cause and effect)
“The actual incidence of statin-exacerbated myasthenia is unknown, and only a handful of reports of statin-associated myasthenia gravis have ever been described. Out of six published case reports, only five patients were noted to have some degree of recovery and only one patient had a complete recovery upon termination of statin therapy.
How statins could appear to exacerbate MG is unclear. It is possible that the mechanism actually reflects a ‘double hit’ phenomenon of defective neuromuscular transmission secondary to antibody-mediated postsynaptic acetylcholine receptor dysfunction in combination with a statin-induced myopathy.
The clear development of a statin myopathy with simvastatin treatment before the onset of myasthenia in our patient is consistent with the possibility of a second (atorvastatin-induced) myopathy coalescing with the onset of myasthenia gravis. The symptomatic improvement that followed his withdrawal from atorvastatin treatment resulted from the resolution of this statin myopathy.
We also considered other potential causes of deterioration such as sepsis, steroid-induced worsening of MG, steroid myopathy, and cholinergic crisis, but we considered their development less likely based on clinical grounds.
We cannot rule out completely the possibility that the worsening of our patient’s MG simply reflected a progression of his MG. However, the clinical course of his condition, as well as the statin-induced proximal limb pain and weakness (without bulbar features) he experienced before his presentation, raises at the very least the possibility that a component of his initial deterioration was statin related.
Similarly, we note that his improvement could have reflected the immunosuppressive effects of therapy for his MG rather than the withdrawal of his atorvastatin treatment. It seems probable, however, that both factors played a significant role in the improvement of his clinical state.
The development of other autoimmune disorders such as dermatomyositis, polymyalgia rheumatica, vasculitis, and Lupus-like syndrome upon initiation of statin therapy raises the possibility that in predisposed individuals, statins may precipitate an immunological trigger that is analogous to penicillamine-induced MG although clearly different in temporal respect. However, given the paucity of reports and the widespread use of statins, the possibility of chance association cannot be excluded still.”
From Statin-associated weakness in myasthenia gravis: a case report11.
11d—Main “take-away” lessons of this case report
“This infant met the diagnostic criteria of the Medical Task Force on Anencephaly. Therefore, she was the longest surviving anencephalic infant who did not require any life-sustaining treatments such as intubation or feeding tubes. Knowing this rare possibility, the physician and family should make goal-oriented decisions on how to care for the infant. The provider should offer immunizations and well childcare to each family if the infant survives the immediate newborn period. This case should affect the practice of physicians who interact with expectant mothers of a child affected by anencephaly.”
From Prolonged unassisted survival in an infant with anencephaly12.
Training
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