31
MOHAMMED V DE RABAT
FACULTE DE MEDECINE ET DE PHARMACIE - RABAT
DOYENS HONORAIRES :
1962 – 1969 : Professeur Abdelmalek FARAJ 1969 – 1974 : Professeur Abdellatif BERBICH 1974 – 1981 : Professeur Bachir LAZRAK 1981 – 1989 : Professeur Taieb CHKILI
1989 – 1997 : Professeur Mohamed Tahar ALAOUI 1997 – 2003 : Professeur Abdelmajid BELMAHI 2003 - 2013 : Professeur Najia HAJJAJ – HASSOUNI
ADMINISTRATION :
Doyen
Professeur Mohamed ADNAOUI
Vice-Doyen chargé des Affaires Académiques et estudiantines Professeur Brahim LEKEHAL
Vice-Doyen chargé de la Recherche et de la Coopération Professeur Toufiq DAKKA
Vice-Doyen chargé des Affaires Spécifiques à la Pharmacie Professeur Jamal TAOUFIK
Secrétaire Général
1 - ENSEIGNANTS-CHERCHEURS MEDECINS ET PHARMACIENS
PROFESSEURS :
DECEMBRE 1984
Pr. MAAOUNI Abdelaziz Médecine Interne – Clinique Royale
Pr. MAAZOUZI Ahmed Wajdi Anesthésie -Réanimation
Pr. SETTAF Abdellatif Pathologie Chirurgicale
NOVEMBRE ET DECEMBRE 1985
Pr. BENSAID Younes Pathologie Chirurgicale
JANVIER, FEVRIER ET DECEMBRE 1987
Pr. LACHKAR Hassan Médecine Interne
Pr. YAHYAOUI Mohamed Neurologie
DECEMBRE 1989
Pr. ADNAOUI Mohamed Médecine Interne –Doyen de la FMPR
Pr. OUAZZANI Taïbi Mohamed Réda Neurologie
JANVIER ET NOVEMBRE 1990
Pr. HACHIM Mohammed* Médecine-Interne
Pr. KHARBACH Aîcha Gynécologie -Obstétrique
Pr. TAZI Saoud Anas Anesthésie Réanimation
FEVRIER AVRIL JUILLET ET DECEMBRE 1991 Pr. AZZOUZI Abderrahim Anesthésie Réanimation- Doyen de FMPO
Pr. BAYAHIA Rabéa Néphrologie
Pr. BELKOUCHI Abdelkader Chirurgie Générale
Pr. BENCHEKROUN Belabbes Abdellatif Chirurgie Générale
Pr. BENSOUDA Yahia Pharmacie galénique
Pr. BERRAHO Amina Ophtalmologie
Pr. BEZAD Rachid Gynécologie Obstétrique Méd. Chef Maternité des
Orangers
Pr. CHERRAH Yahia Pharmacologie
Pr. CHOKAIRI Omar Histologie Embryologie
Pr. KHATTAB Mohamed Pédiatrie
Pr. SOULAYMANI Rachida Pharmacologie- Dir. du Centre National PV Rabat Pr. TAOUFIK Jamal Chimie thérapeutique V.D à la pharmacie+Dir. du CEDOC +
DECEMBRE 1992
Pr. AHALLAT Mohamed Chirurgie Générale Doyen de FMPT
Pr. BENSOUDA Adil Anesthésie Réanimation
Pr. CHAHED OUAZZANI Laaziza Gastro-Entérologie
Pr. CHRAIBI Chafiq Gynécologie Obstétrique
Pr. EL OUAHABI Abdessamad Neurochirurgie
Pr. FELLAT Rokaya Cardiologie
Pr. GHAFIR Driss* Médecine Interne
Pr. JIDDANE Mohamed Anatomie
Pr. TAGHY Ahmed Chirurgie Générale
Pr. ZOUHDI Mimoun Microbiologie
MARS 1994
Pr. BENJAAFAR Noureddine Radiothérapie
Pr. BEN RAIS Nozha Biophysique
Pr. CAOUI Malika Biophysique
Pr. CHRAIBI Abdelmjid
Endocrinologie et Maladies Métaboliques Doyen de la
FMPA
Pr. EL AMRANI Sabah Gynécologie Obstétrique
Pr. EL BARDOUNI Ahmed Traumato-Orthopédie
Pr. EL HASSANI My Rachid Radiologie
Pr. ERROUGANI Abdelkader Chirurgie Générale – Directeur du CHIS-Rabat
Pr. ESSAKALI Malika Immunologie
Pr. ETTAYEBI Fouad Chirurgie Pédiatrique
Pr. HASSAM Badredine Dermatologie
Pr. IFRINE Lahssan Chirurgie Générale
Pr. MAHFOUD Mustapha Traumatologie – Orthopédie
Pr. RHRAB Brahim Gynécologie –Obstétrique
Pr. SENOUCI Karima Dermatologie
MARS 1994
Pr. ABBAR Mohamed* Urologie Directeur Hôpital My Ismail Meknès Pr. ABDELHAK M’barek Chirurgie – Pédiatrique
Pr. BENTAHILA Abdelali Pédiatrie
Pr. BENYAHIA Mohammed Ali Gynécologie – Obstétrique Pr. BERRADA Mohamed Saleh Traumatologie – Orthopédie Pr. CHERKAOUI Lalla Ouafae Ophtalmologie
Pr. LAKHDAR Amina Gynécologie Obstétrique
Pr. MOUANE Nezha Pédiatrie
MARS 1995
Pr. ABOUQUAL Redouane Réanimation Médicale
Pr. AMRAOUI Mohamed Chirurgie Générale
Pr. BARGACH Samir Gynécologie Obstétrique Pr. DRISSI KAMILI Med Nordine* Anesthésie Réanimation
Pr. EL MESNAOUI Abbes Chirurgie Générale
Pr. ESSAKALI HOUSSYNI Leila Oto-Rhino-Laryngologie
Pr. HDA Abdelhamid* Cardiologie Inspecteur du Service de Santé des FAR Pr. IBEN ATTYA ANDALOUSSI Ahmed Urologie
Pr. OUAZZANI CHAHDI Bahia Ophtalmologie
Pr. SEFIANI Abdelaziz Génétique
Pr. ZEGGWAGH Amine Ali Réanimation Médicale
DECEMBRE 1996
Pr. AMIL Touriya* Radiologie
Pr. BELKACEM Rachid Chirurgie Pédiatrie
Pr. BOULANOUAR Abdelkrim Ophtalmologie Pr. EL ALAMI EL FARICHA EL Hassan Chirurgie Générale
Pr. GAOUZI Ahmed Pédiatrie
Pr. MAHFOUDI M’barek* Radiologie
Pr. OUZEDDOUN Naima Néphrologie
Pr. ZBIR EL Mehdi* Cardiologie DirecteurHôp.Mil. d’Instruction Med V Rabat
NOVEMBRE 1997
Pr. ALAMI Mohamed Hassan Gynécologie-Obstétrique
Pr. BEN SLIMANE Lounis Urologie
Pr. BIROUK Nazha Neurologie
Pr. ERREIMI Naima Pédiatrie
Pr. FELLAT Nadia Cardiologie
Pr. KADDOURI Noureddine Chirurgie Pédiatrique
Pr. KOUTANI Abdellatif Urologie
Pr. LAHLOU Mohamed Khalid Chirurgie Générale
Pr. MAHRAOUI CHAFIQ Pédiatrie
Pr. TOUFIQ Jallal Psychiatrie Directeur Hôp.Ar-razi Salé
Pr. YOUSFI MALKI Mounia Gynécologie Obstétrique
NOVEMBRE 1998
Pr. BENOMAR ALI Neurologie Doyen de la FMP Abulcassis Pr. BOUGTAB Abdesslam Chirurgie Générale
Pr. ER RIHANI Hassan Oncologie Médicale
Pr. BENKIRANE Majid* Hématologie
JANVIER 2000
Pr. ABID Ahmed* Pneumo-phtisiologie
Pr. AIT OUAMAR Hassan Pédiatrie
Pr. BENJELLOUN Dakhama Badr.Sououd Pédiatrie
Pr. BOURKADI Jamal-Eddine Pneumo-phtisiologie Directeur Hôp. My Youssef Pr. CHARIF CHEFCHAOUNI Al Montacer Chirurgie Générale
Pr. ECHARRAB El Mahjoub Chirurgie Générale Pr. EL FTOUH Mustapha Pneumo-phtisiologie
Pr. EL MOSTARCHID Brahim* Neurochirurgie
Pr. MAHMOUDI Abdelkrim* Anesthésie-Réanimation
Pr. TACHINANTE Rajae Anesthésie-Réanimation
Pr. TAZI MEZALEK Zoubida Médecine Interne
NOVEMBRE 2000
Pr. AIDI Saadia Neurologie
Pr. AJANA Fatima Zohra Gastro-Entérologie
Pr. BENAMR Said Chirurgie Générale
Pr. CHERTI Mohammed Cardiologie
Pr. ECH-CHERIF EL KETTANI Selma Anesthésie-Réanimation
Pr. EL HASSANI Amine Pédiatrie - Directeur Hôp.Cheikh Zaid
Pr. EL KHADER Khalid Urologie
Pr. EL MAGHRAOUI Abdellah* Rhumatologie
Pr. GHARBI Mohamed El Hassan Endocrinologie et Maladies Métaboliques
Pr. MDAGHRI ALAOUI Asmae Pédiatrie
Pr. ROUIMI Abdelhadi* Neurologie
DECEMBRE 2000
Pr.ZOHAIR ABDELLAH * ORL
Pr. BALKHI Hicham* Anesthésie-Réanimation
Pr. BENABDELJLIL Maria Neurologie
Pr. BENAMAR Loubna Néphrologie
Pr. BENAMOR Jouda Pneumo-phtisiologie
Pr. BENELBARHDADI Imane Gastro-Entérologie
Pr. BENNANI Rajae Cardiologie
Pr. BENOUACHANE Thami Pédiatrie
Pr. BEZZA Ahmed* Rhumatologie
Pr. BOUCHIKHI IDRISSI Med Larbi Anatomie
Pr. BOUMDIN El Hassane* Radiologie
Pr. CHAT Latifa Radiologie
Pr. DAALI Mustapha* Chirurgie Générale
Pr. DRISSI Sidi Mourad* Radiologie
Pr. EL HIJRI Ahmed Anesthésie-Réanimation
Pr. EL MAAQILI Moulay Rachid Neuro-Chirurgie
Pr. EL MADHI Tarik Chirurgie-Pédiatrique
Pr. EL OUNANI Mohamed Chirurgie Générale
Pr. ETTAIR Said Pédiatrie - Directeur Hôp. d’EnfantsRabat
Pr. GAZZAZ Miloudi* Neuro-Chirurgie
Pr. HRORA Abdelmalek Chirurgie Générale
Pr. KABIRI EL Hassane* Chirurgie Thoracique Pr. LAMRANI Moulay Omar Traumatologie Orthopédie
Pr. LEKEHAL Brahim Chirurgie Vasculaire Périphérique
Pr. MAHASSIN Fattouma* Médecine Interne
Pr. MEDARHRI Jalil Chirurgie Générale
Pr. MIKDAME Mohammed* Hématologie Clinique
Pr. MOHSINE Raouf Chirurgie Générale
Pr. NOUINI Yassine Urologie - Directeur Hôpital Ibn Sina
Pr. SABBAH Farid Chirurgie Générale
Pr. SEFIANI Yasser Chirurgie Vasculaire Périphérique Pr. TAOUFIQ BENCHEKROUN Soumia Pédiatrie
DECEMBRE 2002
Pr. AL BOUZIDI Abderrahmane* Anatomie Pathologique
Pr. AMEUR Ahmed * Urologie
Pr. AMRI Rachida Cardiologie
Pr. AOURARH Aziz* Gastro-Entérologie
Pr. BAMOU Youssef * Biochimie-Chimie
Pr. BELMEJDOUB Ghizlene* Endocrinologie et Maladies Métaboliques
Pr. BENZEKRI Laila Dermatologie
Pr. BENZZOUBEIR Nadia Gastro-Entérologie
Pr. BERNOUSSI Zakiya Anatomie Pathologique Pr. BICHRA Mohamed Zakariya* Psychiatrie
Pr. CHOHO Abdelkrim * Chirurgie Générale
Pr. CHKIRATE Bouchra Pédiatrie
Pr. EL ALAMI EL Fellous Sidi Zouhair Chirurgie Pédiatrique
Pr. EL HAOURI Mohamed * Dermatologie
Pr. FILALI ADIB Abdelhai Gynécologie Obstétrique
Pr. HAJJI Zakia Ophtalmologie
Pr. IKEN Ali Urologie
Pr. JAAFAR Abdeloihab* Traumatologie Orthopédie
Pr. KRIOUILE Yamina Pédiatrie
Pr. MABROUK Hfid* Traumatologie Orthopédie
Pr. MOUSSAOUI RAHALI Driss* Gynécologie Obstétrique
Pr. OUJILAL Abdelilah Oto-Rhino-Laryngologie
Pr. RACHID Khalid * Traumatologie Orthopédie
Pr. RAISS Mohamed Chirurgie Générale
Pr. RGUIBI IDRISSI Sidi Mustapha* Pneumo-phtisiologie
Pr. RHOU Hakima Néphrologie
Pr. SIAH Samir * Anesthésie Réanimation
Pr. THIMOU Amal Pédiatrie
JANVIER 2004
Pr. ABDELLAH El Hassan Ophtalmologie
Pr. AMRANI Mariam Anatomie Pathologique
Pr. BENBOUZID Mohammed Anas Oto-Rhino-Laryngologie
Pr. BENKIRANE Ahmed* Gastro-Entérologie
Pr. BOULAADAS Malik Stomatologie et Chirurgie Maxillo-faciale
Pr. BOURAZZA Ahmed* Neurologie
Pr. CHAGAR Belkacem* Traumatologie Orthopédie
Pr. CHERRADI Nadia Anatomie Pathologique
Pr. EL FENNI Jamal* Radiologie
Pr. EL HANCHI ZAKI Gynécologie Obstétrique
Pr. EL KHORASSANI Mohamed Pédiatrie Pr. EL YOUNASSI Badreddine* Cardiologie
Pr. HACHI Hafid Chirurgie Générale
Pr. JABOUIRIK Fatima Pédiatrie
Pr. KHARMAZ Mohamed Traumatologie Orthopédie
Pr. MOUGHIL Said Chirurgie Cardio-Vasculaire
Pr. OUBAAZ Abdelbarre * Ophtalmologie
Pr. TARIB Abdelilah* Pharmacie Clinique
Pr. TIJAMI Fouad Chirurgie Générale
Pr. ZARZUR Jamila Cardiologie
JANVIER 2005
Pr. ABBASSI Abdellah Chirurgie Réparatrice et Plastique Pr. AL KANDRY Sif Eddine* Chirurgie Générale
Pr. ALLALI Fadoua Rhumatologie
Pr. AMAZOUZI Abdellah Ophtalmologie
Pr. AZIZ Noureddine* Radiologie
Pr. BAHIRI Rachid Rhumatologie Directeur Hôp. Al Ayachi Salé
Pr. BARKAT Amina Pédiatrie
Pr. BENYASS Aatif Cardiologie
Pr. DOUDOUH Abderrahim* Biophysique
Pr. EL HAMZAOUI Sakina * Microbiologie
Pr. HAJJI Leila Cardiologie (mise en disponibilité
Pr. HESSISSEN Leila Pédiatrie
Pr. JIDAL Mohamed* Radiologie
Pr. LAAROUSSI Mohamed Chirurgie Cardio-vasculaire
Pr. LYAGOUBI Mohammed Parasitologie
Pr. RAGALA Abdelhak Gynécologie Obstétrique
Pr. SBIHI Souad Histo-Embryologie Cytogénétique
AVRIL 2006
Pr. ACHEMLAL Lahsen* Rhumatologie
Pr. AKJOUJ Said* Radiologie
Pr. BELMEKKI Abdelkader* Hématologie
Pr. BENCHEIKH Razika O.R.L
Pr. BIYI Abdelhamid* Biophysique
Pr. BOUHAFS Mohamed El Amine Chirurgie - Pédiatrique
Pr. BOULAHYA Abdellatif* Chirurgie Cardio – Vasculaire. Pr. CHENGUETI ANSARI Anas Gynécologie Obstétrique
Pr. DOGHMI Nawal Cardiologie
Pr. FELLAT Ibtissam Cardiologie
Pr. FAROUDY Mamoun Anesthésie Réanimation
Pr. HARMOUCHE Hicham Médecine Interne
Pr. HANAFI Sidi Mohamed* Anesthésie Réanimation Pr. IDRISS LAHLOU Amine* Microbiologie
Pr. JROUNDI Laila Radiologie
Pr. KARMOUNI Tariq Urologie
Pr. KILI Amina Pédiatrie
Pr. KISRA Hassan Psychiatrie
Pr. KISRA Mounir Chirurgie – Pédiatrique
Pr. LAATIRIS Abdelkader* Pharmacie Galénique Pr. LMIMOUNI Badreddine* Parasitologie
Pr. MANSOURI Hamid* Radiothérapie
Pr. OUANASS Abderrazzak Psychiatrie
Pr. SAFI Soumaya* Endocrinologie
Pr. SEKKAT Fatima Zahra Psychiatrie
Pr. SOUALHI Mouna Pneumo – Phtisiologie
Pr. TELLAL Saida* Biochimie
Pr. ZAHRAOUI Rachida Pneumo – Phtisiologie
DECEMBRE 2006
Pr SAIR Khalid Chirurgie générale Dir. Hôp.Av.Marrakech
OCTOBRE 2007
Pr. ABIDI Khalid Réanimation médicale
Pr. ACHACHI Leila Pneumo phtisiologie
Pr. ACHOUR Abdessamad* Chirurgie générale
Pr. AIT HOUSSA Mahdi * Chirurgie cardio vasculaire Pr. AMHAJJI Larbi * Traumatologie orthopédie
Pr. AOUFI Sarra Parasitologie
Pr. BAITE Abdelouahed * Anesthésie réanimation Directeur ERSSM Pr. BALOUCH Lhousaine * Biochimie-chimie
Pr. BOUTIMZINE Nourdine Ophtalmologie Pr. CHERKAOUI Naoual * Pharmacie galénique Pr. EHIRCHIOU Abdelkader * Chirurgie générale
Pr. EL BEKKALI Youssef * Chirurgie cardio-vasculaire Pr. EL ABSI Mohamed Chirurgie générale
Pr. EL MOUSSAOUI Rachid Anesthésie réanimation
Pr. EL OMARI Fatima Psychiatrie
Pr. GHARIB Noureddine Chirurgie plastique et réparatrice
Pr. HADADI Khalid * Radiothérapie
Pr. ICHOU Mohamed * Oncologie médicale
Pr. ISMAILI Nadia Dermatologie
Pr. KEBDANI Tayeb Radiothérapie
Pr. LALAOUI SALIM Jaafar * Anesthésie réanimation
Pr. LOUZI Lhoussain * Microbiologie
Pr. MADANI Naoufel Réanimation médicale
Pr. MAHI Mohamed * Radiologie
Pr. MARC Karima Pneumo phtisiologie
Pr. MASRAR Azlarab Hématologie biologique
Pr. MRANI Saad * Virologie
Pr. OUZZIF Ez zohra * Biochimie-chimie
Pr. RABHI Monsef * Médecine interne
Pr. RADOUANE Bouchaib* Radiologie
Pr. SEFFAR Myriame Microbiologie
Pr. SEKHSOKH Yessine * Microbiologie
Pr. SIFAT Hassan * Radiothérapie
Pr. TABERKANET Mustafa * Chirurgie vasculaire périphérique
Pr. TACHFOUTI Samira Ophtalmologie
Pr. TAJDINE Mohammed Tariq* Chirurgie générale Pr. TANANE Mansour * Traumatologie-orthopédie
Pr. TLIGUI Houssain Parasitologie
Pr. TOUATI Zakia Cardiologie
DECEMBRE 2008
Pr TAHIRI My El Hassan* Chirurgie Générale
MARS 2009
Pr. ABOUZAHIR Ali * Médecine interne
Pr. AGADR Aomar * Pédiatrie
Pr. AIT ALI Abdelmounaim * Chirurgie Générale Pr. AIT BENHADDOU El Hachmia Neurologie
Pr. AKHADDAR Ali * Neuro-chirurgie
Pr. ALLALI Nazik Radiologie
Pr. ARKHA Yassir Neuro-chirurgie Directeur Hôp.des Spécialités Pr. BELYAMANI Lahcen* Anesthésie Réanimation
Pr. BJIJOU Younes Anatomie
Pr. BOUHSAIN Sanae * Biochimie-chimie
Pr. BOUI Mohammed * Dermatologie
Pr. BOUNAIM Ahmed * Chirurgie Générale
Pr. BOUSSOUGA Mostapha * Traumatologie-orthopédie
Pr. CHTATA Hassan Toufik * Chirurgie Vasculaire Périphérique
Pr. DOGHMI Kamal * Hématologie clinique
Pr. EL MALKI Hadj Omar Chirurgie Générale Pr. EL OUENNASS Mostapha* Microbiologie
Pr. ENNIBI Khalid * Médecine interne
Pr. FATHI Khalid Gynécologie obstétrique
Pr. HASSIKOU Hasna * Rhumatologie
Pr. KABBAJ Nawal Gastro-entérologie
Pr. KABIRI Meryem Pédiatrie
Pr. KARBOUBI Lamya Pédiatrie
Pr. LAMSAOURI Jamal * Chimie Thérapeutique
Pr. MARMADE Lahcen Chirurgie Cardio-vasculaire
Pr. MESKINI Toufik Pédiatrie
Pr. MESSAOUDI Nezha * Hématologie biologique
Pr. MSSROURI Rahal Chirurgie Générale
Pr. NASSAR Ittimade Radiologie
Pr. OUKERRAJ Latifa Cardiologie
Pr. RHORFI Ismail Abderrahmani * Pneumo-Phtisiologie
OCTOBRE 2010
Pr. ALILOU Mustapha Anesthésie réanimation
Pr. AMEZIANE Taoufiq* Médecine Interne
Pr. BELAGUID Abdelaziz Physiologie
Pr. CHADLI Mariama* Microbiologie
Pr. CHEMSI Mohamed* Médecine Aéronautique
Pr. DAMI Abdellah* Biochimie- Chimie
Pr. DARBI Abdellatif* Radiologie
Pr. DENDANE Mohammed Anouar Chirurgie Pédiatrique
Pr. EL HAFIDI Naima Pédiatrie
Pr. EL KHARRAS Abdennasser* Radiologie
Pr. EL MAZOUZ Samir Chirurgie Plastique et Réparatrice
Pr. EL SAYEGH Hachem Urologie
Pr. ERRABIH Ikram Gastro-Entérologie
Pr. LAMALMI Najat Anatomie Pathologique
Pr. MOSADIK Ahlam Anesthésie Réanimation
Pr. MOUJAHID Mountassir* Chirurgie Générale
Pr. NAZIH Mouna* Hématologie
DECEMBRE 2010
Pr.ZNATI Kaoutar Anatomie Pathologique
MAI 2012
Pr. AMRANI Abdelouahed Chirurgie pédiatrique Pr. ABOUELALAA Khalil * Anesthésie Réanimation Pr. BENCHEBBA Driss * Traumatologie-orthopédie
Pr. DRISSI Mohamed * Anesthésie Réanimation
Pr. EL ALAOUI MHAMDI Mouna Chirurgie Générale Pr. EL KHATTABI Abdessadek * Médecine Interne Pr. EL OUAZZANI Hanane * Pneumophtisiologie
Pr. ER-RAJI Mounir Chirurgie Pédiatrique
Pr. JAHID Ahmed Anatomie Pathologique
Pr. MEHSSANI Jamal * Psychiatrie
Pr. RAISSOUNI Maha * Cardiologie
* Enseignants Militaires FEVRIER 2013
Pr.AHID Samir Pharmacologie
Pr.AIT EL CADI Mina Toxicologie
Pr.AMRANI HANCHI Laila Gastro-Entérologie
Pr.AMOR Mourad Anesthésie Réanimation
Pr.AWAB Almahdi Anesthésie Réanimation
Pr.BELAYACHI Jihane Réanimation Médicale
Pr.BELKHADIR Zakaria Houssain Anesthésie Réanimation
Pr.BENCHEKROUN Laila Biochimie-Chimie
Pr.BENKIRANE Souad Hématologie
Pr.BENNANA Ahmed* Informatique Pharmaceutique
Pr.BENSGHIR Mustapha * Anesthésie Réanimation
Pr.BENYAHIA Mohammed * Néphrologie
Pr.BOUATIA Mustapha Chimie Analytique et Bromatologie Pr.BOUABID Ahmed Salim* Traumatologie orthopédie
Pr BOUTARBOUCH Mahjouba Anatomie
Pr.CHAIB Ali * Cardiologie
Pr.DENDANE Tarek Réanimation Médicale
Pr.DINI Nouzha * Pédiatrie
Pr.ECH-CHERIF EL KETTANI Mohamed Ali Anesthésie Réanimation Pr.ECH-CHERIF EL KETTANI Najwa Radiologie
Pr.EL FATEMI NIZARE Neuro-chirurgie
Pr.EL GUERROUJ Hasnae Médecine Nucléaire
Pr.EL JAOUDI Rachid * Toxicologie
Pr.EL KABABRI Maria Pédiatrie
Pr.EL KHANNOUSSI Basma Anatomie Pathologique
Pr.EL KHLOUFI Samir Anatomie
Pr.EL KORAICHI Alae Anesthésie Réanimation
Pr.EN-NOUALI Hassane * Radiologie
Pr.ERRGUIG Laila Physiologie
Pr.FIKRI Meryem Radiologie
Pr.GHFIR Imade Médecine Nucléaire
Pr.IMANE Zineb Pédiatrie
Pr.IRAQI Hind Endocrinologie et maladies métaboliques
Pr.KABBAJ Hakima Microbiologie
Pr.KADIRI Mohamed * Psychiatrie
Pr.MAAMAR Mouna Fatima Zahra Médecine Interne
Pr.MEDDAH Bouchra Pharmacologie
Pr.MELHAOUI Adyl Neuro-chirurgie
Pr.MRABTI Hind Oncologie Médicale
Pr.NEJJARI Rachid Pharmacognosie
Pr.OUBEJJA Houda Chirugie Pédiatrique
Pr.OUKABLI Mohamed * Anatomie Pathologique
Pr.RAHALI Younes Pharmacie Galénique
Pr.RATBI Ilham Génétique
Pr.RAHMANI Mounia Neurologie
Pr.REDA Karim * Ophtalmologie
Pr.REGRAGUI Wafa Neurologie
Pr.RKAIN Hanan Physiologie
Pr.ROSTOM Samira Rhumatologie
Pr.ROUAS Lamiaa Anatomie Pathologique
Pr.ROUIBAA Fedoua * Gastro-Entérologie
Pr SALIHOUN Mouna Gastro-Entérologie
Pr.SAYAH Rochde Chirurgie Cardio-Vasculaire
Pr.SEDDIK Hassan * Gastro-Entérologie
Pr.ZERHOUNI Hicham Chirurgie Pédiatrique
AVRIL 2013
Pr.EL KHATIB MOHAMED KARIM * Stomatologie et Chirurgie Maxillo-faciale
MAI 2013
Pr.BOUSLIMAN Yassir Toxicologie
MARS 2014
Pr. ACHIR Abdellah Chirurgie Thoracique
Pr.BENCHAKROUN Mohammed * Traumatologie- Orthopédie
Pr.BOUCHIKH Mohammed Chirurgie Thoracique
Pr. EL KABBAJ Driss * Néphrologie
Pr. EL MACHTANI IDRISSI Samira * Biochimie-Chimie
Pr. HARDIZI Houyam Histologie- Embryologie-Cytogénétique
Pr. HASSANI Amale * Pédiatrie
Pr. HERRAK Laila Pneumologie
Pr. JANANE Abdellah * Urologie
Pr. JEAIDI Anass * Hématologie Biologique
Pr. KOUACH Jaouad* Gynécologie-Obstétrique
Pr. LEMNOUER Abdelhay* Microbiologie
Pr. MAKRAM Sanaa * Pharmacologie
Pr. OULAHYANE Rachid* Chirurgie Pédiatrique
Pr. RHISSASSI Mohamed Jaafar CCV
Pr. SABRY Mohamed* Cardiologie
Pr. SEKKACH Youssef* Médecine Interne
Pr. TAZI MOUKHA Zakia Gynécologie-Obstétrique
AVRIL 2014
PROFESSEURS AGREGES :
DECEMBRE 2014
Pr. ABILKASSEM Rachid* Pédiatrie
Pr. AIT BOUGHIMA Fadila Médecine Légale
Pr. BEKKALI Hicham * Anesthésie-Réanimation
Pr. BENAZZOU Salma Chirurgie Maxillo-Faciale
Pr. BOUABDELLAH Mounya Biochimie-Chimie
Pr. BOUCHRIK Mourad* Parasitologie
Pr. DERRAJI Soufiane* Pharmacie Clinique
Pr. DOBLALI Taoufik* Microbiologie
Pr. EL AYOUBI EL IDRISSI Ali Anatomie
Pr. EL GHADBANE Abdedaim Hatim* Anesthésie-Réanimation
Pr. EL MARJANY Mohammed* Radiothérapie
Pr. FEJJAL Nawfal Chirurgie Réparatrice et Plastique
Pr. JAHIDI Mohamed* O.R.L
Pr. LAKHAL Zouhair* Cardiologie
Pr. OUDGHIRI NEZHA Anesthésie-Réanimation
Pr. RAMI Mohamed Chirurgie Pédiatrique
Pr. SABIR Maria Psychiatrie
Pr. SBAI IDRISSI Karim* Médecine préventive, santé publique et Hyg.
AOUT 2015
Pr. MEZIANE Meryem Dermatologie
Pr. TAHRI Latifa Rhumatologie
JANVIER 2016
Pr. BENKABBOU Amine Chirurgie Générale
Pr. EL ASRI Fouad* Ophtalmologie
Pr. ERRAMI Noureddine* O.R.L
Pr. NITASSI Sophia O.R.L
JUIN 2017
Pr. ABI Rachid* Microbiologie
Pr. ASFALOU Ilyasse* Cardiologie
Pr. BOUAYTI El Arbi* Médecine préventive, santé publique et Hyg.
Pr. BOUTAYEB Saber Oncologie Médicale
Pr. EL GHISSASSI Ibrahim Oncologie Médicale
Pr. OURAINI Saloua* O.R.L
Pr. RAZINE Rachid Médecine préventive, santé publique et Hyg.
Pr. ZRARA Abdelhamid* Immunologie
2 - ENSEIGNANTS-CHERCHEURS SCIENTIFIQUES
PROFESSEURS/Prs. HABILITES
Pr. ABOUDRAR Saadia Physiologie
Pr. ALAMI OUHABI Naima Biochimie-chimie
Pr. ALAOUI KATIM Pharmacologie
Pr. ALAOUI SLIMANI Lalla Naïma Histologie-Embryologie
Pr. ANSAR M’hammed Chimie Organique et Pharmacie Chimique
Pr .BARKIYOU Malika Histologie-Embryologie
Pr. BOUHOUCHE Ahmed Génétique Humaine
Pr. BOUKLOUZE Abdelaziz Applications Pharmaceutiques Pr. CHAHED OUAZZANI Lalla Chadia Biochimie-chimie
Pr. DAKKA Taoufiq Physiologie
Pr. FAOUZI Moulay El Abbes Pharmacologie
Pr. IBRAHIMI Azeddine Biologie moléculaire/Biotechnologie
Pr. KHANFRI Jamal Eddine Biologie
Pr. OULAD BOUYAHYA IDRISSI Med Chimie Organique
Pr. REDHA Ahlam Chimie
Pr. TOUATI Driss Pharmacognosie
Pr. ZAHIDI Ahmed Pharmacologie
Mise à jour le 10/10/2018 Khaled Abdellah
Undertaking this thesis has been a truly life-changing
experience for me and it would not have been possible to do
without the support and guidance that I received from many
people. All of you have empowered me throughout this journey.
To my dear friends
I am thankful for all my friends and colleagues for their
friendship, kindness and invaluable advice and feedback on my
To my family
I would like to say a heartfelt thank you to my Mum, Dad and
my brother for always believing in me and encouraging me to
follow my dreams, and for helping in whatever way they could
during this challenging period. Words can not express how
grateful I am to you for all of the sacrifices that you’ve made on
my behalf. Your prayer for me was what kept me strong and
thankful everyday.
To my wife
You have been by my side throughout this thesis, living every
single minute of it, and without you, I would not have
accomplished this today. I am so grateful that we embarked on
To our Master and Thesis President
Professor B.Chagar
Professor of traumatology and orthopedics
in the military hospital HMV
I gratefully acknowledge Professor CHAGAR for his
encouragement and valuable input. I also want to thank you
To our Master and Thesis Reporter
Professor A.Amrani
Professor of Pediatric surgery
in the children’s hospital of Rabat
I would like to thank my supervisor Professor. AMRANI for
all the support and encouragement he gave me, without his
guidance and constant feedback this study would not have been
achievable. You have been a tremendous mentor for me and your
To our Master and Thesis Judge
Professor M.Raouf
Professor of general surgery
in the national institute of oncology of Rabat
I would like to express my sincere gratitude to my Professor
M.Raouf for accepting to be part of my thesis committe and for
To our Master and Thesis Judge
Professor N.El Hafidi
Professor of pediatrics
in the children’s hospital of Rabat
I would like to thank you for your presence and your valuable
comments and suggestions. But above all, thank you for your
To our Master and Thesis Judge
Professor A.El Hijri
Professor of anesthesiology and reanimation
in Avicenne’s hospital of Rabat
I gratefully acknowledge Professor A.EL Hijri for his presence,
for his encouragement and valuable input. It is an honor to
Abbreviations
AP : Antero-posteriorAI : Acetabular index
BTXA : Botulinum toxin type A
CA : Computed aided
CP : Cerebral palsy
CNS : Central nervous system
CT : Computed tomography
DM : Digital measurement
GABA : G-aminobutyric acid
GMFCS : Gross motor function classification system
HO : Heterotopic ossification
HSA : Head shaft angle
MA : Assisted measurement
MCPHCS : Melbourne cerebral palsy hip classification scale MP : Migration percentage
MRI : Magnetic resonance imaging
NSA : Neck shaft angle
PACS : Picture Archiving and Communication System
PFIA : Proximal femoral interposition arthroplasty
RMI : Reimer migration index
ROM : Range of motion
SCPE : Surveillance of cerebral palsy in Europe
SDRP : Single dose radiation program
SVO : Sub-tronchanteric varus osteotomy
SWASH : Sitting and walking a
THA : Total hip arthroplasty
UMNS : Upper motor neuron syndrome
VDRO : Varus derotational osteotomy
WS : Windswept
List of figures
Figure 1 : Preoperative image : windswept hip deformity. ... 10
Figure 2 : Preoperative radiograph showing left hip dislocation ... 10
Figure 3 : Peroperative images : A : extraperiosteal approach, periosteal excision and release of
musculotendinous attachments. B : interposition arthroplasty –iliopsoas and abductors are sutured to his capsule and femoral stump is covered by vastus lateralis. ... 11
Figure 4 : Proximal head of the femur showing degenerative changes in the cartilage ... 12
Figure 5 : Postoperative image showing improvement in sitting and ROM. ... 12
Figure 6 : Postoperative radiograph of the patient after PFRA surgery. ... 13
Figure 7 : Preoperative image showing crossed legs position. ... 14
Figure 8 : Preoperative radiograph showing bilateral hip dislocation. ... 14
Figure 9 : Peroperative image showing degenerative changes of the cartilage. ... 15
Figure 10 : postoPerative image showing improvement in ROM. ... 16
Figure 11 : Postoperative radiograph of the patient after PFRA surgery. ... 16
Figure 12 : Age of children presenting a neglected hip dislocation ... 18
Figure 13 : Percentage of unilateral and bilateral hip dislocation ... 19
Figure 14 : Number of patients who had previous treatments ( BTXA injections, physiotherapy,
standing program and soft tissue surgery) ... 19
Figure 15 : BTX A injections as an adjuvant treatment to the PFR arthroplasty surgery. ... 20
Figure 16 : Postoperative immobilization treatment ... 20
Figure 17 : Hip displacement (migration percentage >30%) by GMFCS Level ... 26
Figure 18 : Pelvis radiograph of a child with windblown hip deformity. The left hip has adducted and
internally rotated and the right hip is abducted and externally rotated. ... 29
Figure 19 : Preoperative radiograph of a child with cerebral palsy and scoliosis ... 30
Figure 20 : degenerative changes in the femoral head with loss of cartilage ... 36
Figure 21: Migration percentage (MP) is measured by the percentage of the ossified femoral head that
is, lateral to the Perkins line (MP 5 A/D × 100%). AI, acetabular index; H, Hilgenliner’s Line; P, Per- kins Line. (From Dobson F, Boyd RN, Parrott J, et al. Hip surveillance in children with cerebral palsy. Impact on the surgical manage- ment of spastic hip disease ... 41
Figure 22: Measurement of the neck shaft angle ... 42
Figure 24 : (A) Preoperative radiograph of a chronic dislocated hip in a 17-year-old girl. (B)
Postoperative view showing the use of the cancellous screws as a fixation option. ... 50
Figure 25 : Patient with GMFCS V spastic tetraplegic cerebral palsy, painful dislocation of the left
hip and scoliosis. a: dislocation at 15 years of age, total hip arthroplasty on the left (press-fit dual-mobility cup with screw fixation, dysplastic femoral component); c: scoliosis surgery at 17 years of age. ... 52
List of tables
Tableau I: Clinical variables of the patients....7
Introduction ...1 First chapter : Materials and methods ...6 I. Design ...7 II. Patients and methods...7 Second chapter : Results ... 17 Third chapter: Discussion ... 22 I. Natural history of the hip in CP ... 23 II. Hip dislocation risk factors ... 25 1. Growth motor function classification system (GMFCS ) ... 25 2. Spasticity ... 28 3. Contractures ... 28 4. Windswept hip deformity ... 29 5. Scoliosis ... 30 6. Risk Related to Age ... 31 7. Rate of Increase in the MI... 31 8. Muscle Tone and Movement Disorder as a Risk for Hip Subluxation or Dislocation ..
... 31 9. Hip Range of Motion as a Risk Factor ... 32 III. Epidemiology of dislocation ... 33 IV. Diagnosis of dislocation of the hip in CP ... 34 1. Clinical examination ... 34 2. Pain differecences : CP vs DDH ... 36 3. Radiographic evaluation ... 40 V. Treatment of the neglected dislocation of the hip in children with CP ... 45 1. Salvage procedures ... 45 2. Femoral resection arthroplasty ... 45 3. Subtrochanteric valgus osteotomy (SVO) ... 48 4. Hip arthrodesis ... 49 5. Total hip arthroplasty (THA) ... 51
6. Complications ... 53 VI. Prevention of dislocation of the hip in CP ... 56 1. Primary prevention ... 56 2. Secondary prevention ... 65 Conclusion ... 72 Appendix ... 75 Résumés ... 80 References ... 84
1
2
Cerebral palsy (CP) is defined as a static, but often changing disorder of movement and posture due to a defect or lesion to the developing fetal or infant brain. It is a major health problem as it affects 2 to 2.5 out of every 1000 births, making it the most common cause of motor disabilities in childhood. (1) The disorder can result from various insults to different areas within the developing central nervous system (CNS), partially explaining the variety in its clinical presentation. Causes of CP differ to some degree according to their time of onset (in utero, during delivery, during the first two years of life) and their clinical subtype. Although CP can be caused by a single causative factor (e.g. intracranial bleeding, perinatal stroke, congenital malformations, intrauterine infection, extreme prematurity, traumatic brain injury), it is most often caused by the interaction of genetic values and multiple environmental stressors. A specific hypoxic event associated with immediate and irreversible cell death explains the etiology of CP in less than 50%. (2)
The Surveillance of Cerebral Palsy in Europe (SCPE) has classified CP into three main groups : dyskinetic, ataxic, and spastic (70-80%). (1) The SCPE states that at least two of the following clinical signs have to be present in spastic CP : abnormal pattern of posture and/or movement, increased tone, and pathological reflexes. The spastic CP syndromes can be further classified according to their topographic distribution. In bilateral spastic CP both sides of the body are involved whereas in unilateral CP only one side of the body is involved.
The spasticity in a child with CP may cause the leg to be positioned in flexion, adduction, and, commonly, internal rotation. This causes the femoral head to displace laterally, superiorly, and posteriorly in the acetabulum. (3) The acetabular rim becomes deformed and develops a posterosuperior channel (3). In younger children, the acetabulum comprises mainly cartilage, and the hips are at higher risk of instability and deformity than in older children.
3
The severity of CP can be measured by the gross motor function level (GMFCS), a system intended to classify children with CP by their age-specific gross motor activity and aims to determine which level best represents the child’s or youth’s present abilities and limitations. It is important to point that the incidence of hip displacement is about 0% for children at GMFCS level I and about 90% for those at GMFCS level V.(4)
Hip displacement in CP is defined by a migration percentage (MP) superior to 30%, it is caused by an imbalance of forces acting on the hip ; the spastic flexors and adductors are stronger and/or more spastic than the extensors and abductors. (5) External forces caused by gravity might contribute to the imbalance related to the position of the spine, pelvis and leg.
The incidence of hip displacement in cerebral palsy is related to the severity of involvement, varying from 1% in children with spastic hemiplegia, up to 75% in those with spastic quadriplegia. (6)
If left untreated, the neglected displacement may progress to subluxation, secondary acetabular dysplasia, deformity of the femoral head, dislocation and painful degenerative arthritis. (6)
Hip dislocation is a painful and severe complication in children with CP (6). The long-term consequences of dislocation of the hip can be disastrous for individual patients leading to pain and loss of the ability to sit comfortably in up to 50% of cases. Other problems include difficulty with perineal care and personal hygiene, pelvic obliquity and scoliosis, poor sitting balance and loss of the ability to stand and walk.
4
The management of the dislocated hip in CP is a multimodal approach including non surgical treatment, surgical treatment and an effective surveillance program for the prevention of the hip in CP.
In developed countries, dedicated surveillance programs have been shown to be effective in terms of identifying hips at risk and preventing pathologic dislocation.
Non surgical treatments have been directed at either reducing the amount of spasticity or stretching a tight or contracted tendon. Tone-reducing agents include baclofen and diazepam. (7) Botulinum toxin (BTXA) is also an effective drug, It blocks the release of acetylcholine at the neuromuscular junction. (8) It has been most commonly used in the lower extremity in conjunction with serial casting to manage gastrosoleus contractures. (9)
Once subluxation has been identified with a MP superior to 30%, early surgical intervention is indicated. The surgical management of hip abnormalities in children with cerebral palsy can be divided into 3 levels. (10) Level 1 consists of soft tissue releases (e.g adductor tenotomies), intended to prevent or halt subluxation, this type of surgery is performed at a young age because of the relatively low impact of the procedure on the child and their parents/caregivers. Level 2 incorporates bony osteotomies and addresses advanced subluxation or dislocation of the hip associated with acetabular and/or femoral dysplasia. Palliative measures are indicated in the treatment of the complications of the dislocated hip such as pain, arthritis, and these are level 3 surgery. There is still no clear agreement on the threshold for intervention.
5
This is a retrospective study of children with CP with GMFCS level V and Aschworth level IV with neglected dislocated hips who underwent salvage surgery consisting in a proximal femoral resection (PFR).
The purpose of this thesis was to provide further information about : - The management of the neglected dislocated hip in cerebral palsy. - The outcome of PFR for the painful dislocated hip.
- The importance of a reliable surveillance program of the hip to prevent the neglected painful dislocated hip.
6
First chapter :
7
I. Design
This is a retrospective study, of children with cerebral palsy with neglected hip dislocation who underwent PFR to correct this problem. These children are from selected regions of Morocco (Rabat, salé and Meknes). The aim of this study is to describe the management of the neglected dislocated hip in cerebral palsy.
II. Patients and methods
This study included 6 children with cerebral palsy (3 boys and 3 girls) GMFCS level V, with a dislocated hip, who had a PFR surgery, followed between 2016 and 2019 in the orthopedics department in the children’s hospital of Rabat. The total population of children included in our study is represented in Table I.
Tableau I: Clinical variables of the patients.
Age Side GMF CS Spasticity (ashworth) Previous treatments Standing
program Pain ROM Qol Case 1 :
Zakaria 12 Left V IV None - +++ <10° - Case 2 : Meryem 14 Left V IV Physiothera py - +++ <10° - Case 3 : Rihab 13 Left V IV Physiothera py - +++ <20° - Case 4 : Meknes 11 Left V IV Physiothera py - +++ <10° - Case 5 : Abdellah 7 Bila teral V IV None - +++ <10 - Case 6 : Aya 3 year s and ½ Bila teral V IV Physiothera py - +++ <10 -
8
The indications for PFR surgery included intractable pain at rest or disturbing sleep, pain with seating/positioning, problems with perineal hygiene, a neglected hip with dislocation and radiographs, and severe limitation of movement of the hip.
Clinical variables studied included age at the time of surgery, the type of movement disorder, GMFCS level and the spasticity level, pain level, quality of life and range of motion of the hip abduction. Anterior treatments to the surgery were noted : Botulinum toxin injections, soft tissue surgery and physical treatments such as physiotherapy and standing programs.
Inclusion criteria included McCarthy procedure performed in children with cerebral palsy presenting a neglected dislocated hip, all surgeries were performed by the same surgeon. We excluded cases performed in children for diagnoses other than spastic hip dislocation and those with inadequate records.
Preoperative anteroposterior radiographs were used to measure the migration percentage (MP).
The surgical technique used in all children was in accordance with McCarthy et al. (), including extraperiosteal resection of the proximal femur from 3–4 cm below the lesser trochanter. Interposition technique involved suturing the iliopsoas and gluteal muscles to the hip capsule (“closing” the acetabulum) and covering the femoral stump by suturing the vastus lateralis to the muscles and soft tissues on the medial side. The postoperative treatment and immobilization technique consisted in casting, splints and a pillow hip abduction.
9
The postoperative assessment included ROM, quality of life including perineal care, sleeping and seating, and possible complications such as pain after surgery, heterotopic ossification and migration of the stump. Postoperative and the most recent follow-up radiographs were compared to measure hip stability.
The assessment of quality of life changes was done using the following questions posed to the caregivers :
1. Was your child’s pain improved postoperatively?
2. Was your child’s seating tolerance improved postoperatively?
3. Would you recommend this procedure to other caregivers of children with a similar condition to your child ?
10
Case 1 : Patient number 4 : meknes
Figure 1 : Preoperative image : windswept hip deformity.
11
Figure 3 : Peroperative images : A : extraperiosteal approach, periosteal excision and release of musculotendinous attachments. B : interposition arthroplasty –iliopsoas and
12
Figure 4 : Proximal head of the femur showing degenerative changes in the cartilage
13
14
Case 2 : patient number 6
Figure 7 : Preoperative image showing crossed legs position.
15
16
Figure 10 : postoPerative image showing improvement in ROM.
17
Second chapter :
Results
18
Between 2016 and 2019, 6 patients were treated for a neglected dislocated hip with PFR. All children were at GMFCS level V and Ashworth spasticity level IV.
The average age at the time of surgery was 10 years (range 3.5–14). All patients underwent unilateral surgery performed under the same anesthetic protocol. The mean follow up was 23 months (range 6-36). (fig.12) The sex ratio was 1.
Figure 12 : Age of children presenting a neglected hip dislocation
All patients were non-anbulatory with spastic quadriparesis.
2 patients presented a windswept atittude at the clinical examination.
4 patients had a dislocation of the left hip while 2 had bilateral dislocation of both hips.(fig.13)
19
Figure 13 : Percentage of unilateral and bilateral hip dislocation
None of the patients had prior surgical procedures, 4 patients had a physiotherapy program, one patient had both physiotherapy and a standing program, and one patient didn’t have any anterior treatment.(fig.14)
Figure 14 : Number of patients who had previous treatments ( BTXA injections, physiotherapy, standing program and soft tissue surgery)
20
4 patients had BTX A injections as an adjuvant treatment to the surgery to decrease the spasticity of the muscles and to relieve pain in the time of surgery.
(fig.15) .
Figure 15 : BTX A injections as an adjuvant treatment to the PFR arthroplasty surgery.
Postoperative immobilization consisted in casting in 2 patients, splints in 3 patients and a cushion under the knee in one patient. (fig.16)
21
A pain-free hip that did not dislocate and did not require further treatment, classified as a good or fair result, was obtained in all of the surgically treated hips. A significant improvement in perineal care, sitting and transfers was found in all children.
ROM was significantly improved after the PFR surgery and became hypermobile in all children. (Table VII).
Tableau II: Preoperative and postoperative ROM in all children after PFRA surgery
Patient ROM preoperatively ROM postoperatively
1 <10 Hypermobile 2 <10 Hypermobile 3 <20 Hypermobile 4 <10 Hypermobile 5 <10 Hypermobile 6 <10 Hypermobile
In the whole study population, no cases of complications were observed mainly heterotopic ossification and migration of the stump. Only one patient had Indometacine for the prevention of the ossification and 5 patients did not have the treatment. None of the patients had radiotherapy sessions.
22
Third chapter:
Discussion
23
I. Natural history of the hip in CP
In the normal hip, balanced muscle use promotes the symbiotic development of the acetabulum and femoral head. Upright posture and ambulation promotes remodeling of neonatal femoral anteversion. Children with cerebral palsy are born with normal hips. However, these hips are soon subjected to abnormal muscle forces that lead to hip abnormalities. (11)
The ability to ambulate determines the fate of the hips. Children who become independent ambulators by age 5 years develop enough muscle balance to stabilize the hips ; they may develop acetabular dysplasia or femoral head deformities but do not dislocate. Children who ambulate with crutches, walkers, or canes may develop silent and painless subluxation of hips that may not be a clinical issue for years. Nonambulators may begin to dislocate before the age of 7 years. (12)
It is thought that the main muscle deformers of the hip joint are the adductors, hip flexors, and hamstrings. The hip joint has a ball-and-socket configuration that presumably maximizes contact between the femoral head and the acetabulum throughout a wide range of different positions including flexion and extension.
The combination of spastic muscle activity and altered posture redirects the femoral head to the superolateral and posterior aspects of the acetabulum. If the weak abductors and extensors are unable to offset the adductor spasticity, a contracture of the adductors and the inferomedial joint capsule develops in time. The femoral head is directed and restricted to the lateral rim of the socket. The abnormal forces on the chondroepiphysis of the acetabulum presumably lead to suppression of normal growth. Based on computed tomography (CT) scans, the
24
deficiency is usually in the superolateral or posterior aspect of the acetabulum. (13) It is unclear whether the acetabulum is dysplastic or is enlarging. Recent three-dimensional (3D) reconstruction study has shown that, once the hip dislocates, the acetabular deformity becomes global and the volume of the acetabulum decreases in much the same way that a saucer holds less volume than a cup. (14) The greatest deformation of the acetabulum and femoral head occurs when the migration index is 52% to 68%. (15) In cases in which the spasticity of the legs is asymmetric, a windblown deformity develops with the infrapelvic obliquity. The high side usually dislocates, although exceptions do occur.
There are no reports of mirror image articular cartilage lesions on the acetabular side. Regardless of the cause, the combination of remodeling and articular cartilage degeneration produces a femoral head that is not considered to be reconstructable.
In general, the progression of hip dysplasia is gradual, and it usually occurs over a period of several years. It tend to be a permanent process ; once a hip begins to subluxate, it frequently requires treatment to correct. Hips that have a migration index of greater than 50% will not reduce spontaneously and one- third of those will progress to dislocation. (16)
Many children with a dysplastic hip progressing to dislocation will develop a painful hip by early adulthood ; as hip displacement progresses, the articular cartilage of the femoral head degenerates secondary to pressures from the surrounding soft tissues. Pain from hip dysplasia occurs primarily from dislocated hips, because hips that are subluxated were noted to be only slightly more painful than reduced hips.
25
In terms of the onset of hip dysplasia in children with CP, subluxation frequently occurs before the age of 5 years, with the mean age of dislocation occurring around the age of 6 to 7 years. Children with CP are at greatest risk of hip dislocation between 4 and 12 years of age. (17)
Understanding the natural history of hip dysplasia in CP is crucial, because it provides a framework for intervention and prevention.
II. Hip dislocation risk factors
Some parameters are well-known risk factors for hip displacement in children with CP ; these include young age, high GMFCS level, high migration percentage (MP), and Windswept deformity (WS) (18). It is also believed that there is a correlation between hip dislocation, pelvic obliquity and scoliosis, although the relationship remains unclear (19).
1. Growth motor function classification system (GMFCS )
As mentioned before in the definition, the motor function is the hallmark of CP. The movement disorder in CP is clinically characterized as an upper motor neuron syndrome (UMNS) with positive and negative signs. Positive signs, often predominating in clinical examinations, are abnormal phenomena due to absent inhibition from cortical circuits. They include spasticity, dyskinesia, hyperreflexia, retained developmental reactions, and secondary musculoskeletal malformations. Negative signs, on the other hand, reflect the loss or absent development of proper sensorimotor control mechanisms resulting in weakness, poor coordination of movements, poor balance, and walking ability. They can be further divided into impairments of coordination due to deficient programing and paresis because of inadequate muscle activations (although the motor
26
pattern may be correct) during voluntary movements and walking. While the emphasis has been on reducing the effects of spasticity and other positive signs, abnormal programing of various movement behaviors may be more deleterious for motor function (20). Components of the disturbed motor control (impairments) that have been identified include : a low activation of agonist muscles, hyperactive stretch reflexes, excessive coactivation of antagonists, and hypoextensibility of the muscle–tendon complex often overlooked as a major cause of the walking dysfunction (21). (fig.3)
The risk of developing hip subluxation is directly related to the severity of motor impairment as assessed by the GMFCS. By combining 4 studies (3,22-24) that reported indication for subluxation of either greater than 30% or 33% migration, found that there is almost a true linear relationship in increased risk as the severity of GMFCS increases. (fig.17)
27
There is a well-recognized linear relationship between the risk of hip displacement with increasing GMFCS level in children with CP. It is important to point that the incidence of hip displacement is about 0% for children at GMFCS level I and about 90% for those at GMFCS level V. Our results confirm other findings of the markedly increased risk of displacement in children with severe motor impairment and this relationship is clearly illustrated in our study population since all patients with neglected hip dislocation were GMFCS level V. Larnet et al (25) found that children at GMFCS V had a 2.5–3 times higher risk of developing hip displacement compared with children at GMFCS III–IV. They also found that children at GMFCS V had the highest annual incidence already at age 2–3 years and at 7–8 years of age. Later displacement is unlikely, as has been shown by others (26,27), in children with normal hips by this age.
This is in match with our findings, we had one patient (3.5 years) with GMFCS level V who had already developed a hip dislocation, while others were aged respectively 12,14,12.5,11 and 7. The older age of these patients can be explained by the fact that they have neglected hip dislocation that started developing a couple of years previously, because as already noted in the natural history of the hip in cerebral palsy, the evolution can be silent at first.
Unfortunately, we couldn’t study the difference in risk of hip displacement in children at GMFCS V compared to GMFCS III and IV, and the difference between levels III and IV, because of our limited study population.
28
2. Spasticity
The predominant motor disorder in CP is spasticity (28). Maintaining posture and facilitating movement are accomplished by regulating muscle tone (29). The neuromuscular system responds to muscle stretch by altering muscle tone through the stretch reflex, which is important for maintaining balance and controlling motion (30). In spasticity, the stretch reflex increases and intensifies with the velocity of movement (31). Spasticity can lead to postural deficits and motor dysfunction, which limit activity, cause discomfort, and may lead to contractures, skeletal torsion deformities and hip displacement (32). Symmetry of posture in normally developing infants is achieved at 3 months of age; if asymmetry persists beyond this age, long- term gross asymmetry is likely to occur (33). In children with CP, spasticity often starts developing in the second year of life (34), and increases with brain development. (see appendix)
3. Contractures
The growth of the skeleton and the resulting muscle excursion stimulates the growth of the muscle-tendon unit (34). Muscle excursion is reduced in spasticity, which reduces the ability to extend the muscles and causes sustained postures for long periods of time, which can lead to contractures and attenuated muscle growth (34). Contractures also occur as a result of muscle weakness, which in turn can reduce muscle excursion (23). An untreated contracture often causes contractures in adjacent joints. Skeletal growth is influenced by spasticity and contractures, and torsion deformities can develop (23,34). The musculoskeletal situation associated with spasticity, contractures and deformities can be complex to treat, which is why early treatment is essential.
29
4. Windswept hip deformity
The pathology of WS places one hip in adduction and internal rotation, and the contralateral hip in abduction and external rotation (35). windblown hip (Fig. 18) is caused by an adduction deformity of one hip and an abduction deformity of the other hip. It is a deformity that affects primarily nonambulatory children with severe spasticity owing to asymmetric activity of the abductors, adductors, internal rotators, and external rotators. (35) This deformity interferes with the ability of the child to sit properly in a wheelchair.
Figure 18 : Pelvis radiograph of a child with windblown hip deformity. The left hip has adducted and internally rotated and the right hip is abducted and externally rotated. (36)
Young et al. (37) showed an association between WS and asymmetric tone, in which the hip with the stronger adductors is more often adducted or dislocated than is the contralateral hip. Hip dislocation may be a direct cause of WS, and WS may contribute to the development of hip dislocation. WS affects about one-third of children with CP at GMFCS levels III to V (19). It develops most commonly in children younger than 10 years, but the risk is increased up to 20 years of age. WS is difficult to treat and the deviation from the midline is reinforced by gravity. WS impairs the child’s ability to stand and interferes with
30
sitting and lying comfortably (35). The risk of developing WS can be reduced by early treatment of contractures and scoliosis, and early participation in a hip surveillance programme (35). (fig.6)
5. Scoliosis
Scoliosis is a lateral deviation of the spine in the coronal plane caused by muscle imbalance and weakness, and is reinforced by gravity. Scoliosis is associated with pain, pelvic obliquity, sitting problems, pressure ulcers, WS, hip dislocation, and impairments of cardiorespiratory and gastrointestinal functions (19). The risk of hip dislocation increases on the elevated side of the pelvis, when the pelvis is involved in the scoliosis (19). Involvement of the pelvis in scoliosis might be a risk factor for hip dislocation, and vice versa, although the relationship is unclear (19). Children with CP have an increased risk of scoliosis. The reported prevalence is 15-68% (19), with the risk related to the child’s GMFCS level and age (19). The range of prevalence reflects differences in the definition of scoliosis and selection of the study populations. (fig.19)
31
6. Risk Related to Age
To determine the age at highest risk for the development of hip subluxation, combined data on 182 patients from 2 studies (38,39) to report the age at which hips reached 30% or 33% migration. These data show a clear peak between ages 3 and 5 years old. There was further information in 1 paper (40) that evaluated the age at the time of hip dislocation in 38 hips. These data show a later peak, around ages 5 and 6.
7. Rate of Increase in the MI
As these children start with normal hips and then develop hip displacement in childhood, Pruzczinsky et al (41) evaluated the rate at which this displacement occurs. The rate of displacement was reported in 2 papers (23,42) showing a linear relationship increasing from 0.2% per year in GMFCS I to 12% per year in GMFCS V. Also, 1 report found a rate of increase of 8.2% per year in children younger than 5 and 4.4% per year in children older than 5. (42)
8. Muscle Tone and Movement Disorder as a Risk for Hip
Subluxation or Dislocation
None of the authors observed hip subluxation or dislocation in ataxic type of CP. (42,43,44) The last authors calculated the relative risk for hip subluxation as 0 compared with diplegia (44). In spastic diplegic patients, Ha¨gglund et al (23) found hip subluxation in 33.7% and Soo et al (42) in 19.2%. Soo et al stated that in their CP population, 40% of hips are subluxated in dystonia, and 44.4% are subluxated in hypotonia.
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9. Hip Range of Motion as a Risk Factor
Early reports on screening focused on limited hip abduction as an important screening method. (45,46) There are reports indicating that hypotonic hips also subluxate ; therefore, limited hip abduction is not a good screening tool in this population although limitation of abduction is a strong indicator for surveillance in those patients who are spastic or dystonic.
We found that all children included in this study had spastic quadriplegia. Soo et al. (42 ) also reported an increased risk of hip displacement related to CP-subtype with the highest risk in children with spastic quadriplegia (83 %) and dystonic subtype (40 %), compared with spastic diplegia (19 %).
In our serie, windswept deformity was seen in 2 out of 6 children. WS is a severe problem, affecting about one-third of children with CP at GMFCS levels III–V. In most children, WS develops before 10 years of age, but the risk continues up to 20 years of age. The prevention can be done by early inclusion in a hip surveillance program, and early treatment of contractures, the frequency of WS starting in the lower extremities can be reduced.
2 patients had bilateral hip dislocation while the 6 others had unilateral hip dislocation. All patients had a range of motion of hip abduction inferior to 20 degrees.
Spasticity is proven to be a major risk factor for developing hip dislocation. We found that all children with neglected hip dislocation had severe spasticity ( level IV ashworth). Together with the severity of motor function (GMFCS), the severity of spasticity result in hip displacement, if left untreated, develop into major hip dislocation
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III. Epidemiology of dislocation
The incidence and spectrum of hip abnormalities in children with cerebral palsy vary greatly. The reported incidence ranges from 2% to 75%. Current estimates of hip dysplasia in children with CP is approximately 35%, with the prevalence of hip subluxation estimated to be between 25% and 60% and the prevalence of dislocation to be 10% to 15%. (22,47)
These reports include children who have significantly different degrees of neurologic involvement. The severity and pathology ranges from an alteration of gait or muscle contracture to painful neuromuscular dislocation. This wide spectrum raises several challenges for how best to identify the risk of hip deformities and how best to address their needs.
The incidence of hip subluxation and dislocation is known to increase with worsening disease severity as defined by the GMFCS level ; of note, hip displacement was observed in less than 5% of independent ambulators, whereas it was observed in more than 60% of children with no walking capacity.(48) Additionally, the prognosis and incidence of hip disorders is correlated with the ability of a child to pull to standing by 3 years of age; children with the ability to pull to standing have a lower incidence of hip disorders and a better prognosis. (49)
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IV. Diagnosis of dislocation of the hip in CP
1. Clinical examination
A clinical evaluation of the child with cerebral palsy should be part of an ongoing comprehensive surveillance program that incorporates a history of the child’s functional capabilities, clinical examination, and radiographic evaluation. In patients who are ambulatory, the inquiry should detail age-appropriate activities such as standing, walking with assistance, or independent walking. The ability to walk, and the age at which this is achieved, is one of the strongest prognostic indicators of hip problems. Scrutton (50) found that no child who could walk by 30 months developed a hip problem. In children who walked between 30 months and 5 years, the incidence was 15%. Changes in standing or walking should raise the suspicion of possible hip abnormalities. However, this is not the universal finding, because children, especially with severe hemiplegia, can develop hip problems later in life.
In patients who are nonambulatory, changes in mobility, comfort and pain, sitting, contractures, and hygiene difficulties are indicators of hip problems. The input of family, therapists, and other caregivers can be helpful in identifying problems and critical in developing reasonable treatment plans and expectations. Pain is one of the more frequent secondary conditions in CP. A systematic review showed that three of four children with CP were in pain (51). Pain has been found to reduce both self-reported quality of life and participation in life situations (52,53).
