Terapi Hipotermia pada Stroke Hemoragik

Abstract

Terapi antipiretik merupakan salah satu terapi yang dianjurkan untuk pasien stroke karena peningkatan suhu tubuh dianggap berhubungan dengan luaran neurologis yang buruk. Namun demikian, belum ada rekomendasi yang paling tepat untuk kontrol demam baik secara farmakologi maupun mekanik akibat kurangnya temuan klinik.Saat ini, hipotermi terapeutik dianggap satu-satunya metode neuroprotektif yang sukses dalam meningkatkan luaran pasien stroke iskemik. Istilah neuroprotektif disini mengacu pada memelihara atau melindungi cedera saraf yang reversibel agar tidak rusak atau mengalami kematian sel. Metode hipotermi dianggap berpengaruh terhadap sejumlah jalur patofisiologi stroke. Pada penelitian in vitro, hipotermi mencegah edema serebral dan kerusakan sawar darah otak. Selain itu, mencegah aktivasi mikroglia, produksi radikal bebas, dan pelepasan neurotransmitter eksitotoksik serta asam laktat dan piruvat. Selain itu, cerebral metabolic rate (CMR), apoptosis dan respon inflamasi lokal juga berkurang. Hipotermi otak secara lokal dilaporkan menurunkan ekspresi gen interleukin-1b dan pembentukan edema vasogenik pada model perdarahan intraserebrial binatang. Hipotermi terapeutik dianggap lebih efektif bila dimulai lebih awal setelah onset gejala. Durasi hipotermia yang lebih lama juga memiliki efek neuroprotektif persisten dalam jangka waktu lama. Namun demikian, terapi hipotermia memiliki beberapa komplikasi terhadap jantung, paru-paru, immunologi, hematologi, dan metabolik. Komplikasi yang paling sering dilaporkan adalah pneumonia, bradikardi, aritmia, dan trombositopenia. Evaluasi efektivitas hipotermia sulit dievaluasi pada pasien yang tersedasi karena pemeriksaan neurologis harian seringkali membingungkan.

Hypothermia Therapy in Hemorrhagic Stroke

Antipyretic is among one of the suggested therapies for stroke patients. The reason is because increase in body temperature is considered related to bad neurological outcomes. However, there is no best recommendation available for controlling the temperature, neither pharmacologically nor mechanically due to less clinical practices findings available. Currently, therapeutic hypothermia is considered as the one and only successful neuroprotective in enhancing the ischemic strokes patients’ outcomes. The term neuroprotective refers to protecting or conserving various types of reversible neurological injuries from damage or further cell impairment. In vitro studies showed hypothermia prevent cerebral edema and blood brain barrier damage, as well as successfully proven effective in preventing microglia activation, free radical production, and release of exotoxic neurotransmitters, lactic acid and piruvate. In addition, cerebral metabolite rate (CMR), apoptosis, and local inflammatory response are also decreased. Local brain hypothermia is reported could lowering the 1b-interleukin gen expression and establishment of vasogenic edema among animal models with intracerebral hemorrhage. Therapeutic hypothermia is considered highly effective when initiated early in subsequent to the symptom onset. Longer duration of cooling is related to a more persistent neuroprotective effect in long periode. Despite its effectiveness, therapeutic hypothermia could generate several complications affecting the heart, lung, immunology, hepatology and metabolic states. The most common complications are pneumonia, bradicardia, arrhythmia, and thrombocytopenia. Evaluation to the effectiveness of hypothermia is difficult to measure in sedated patients due to difficulty in defining the patient’s neurological states on day to day bases